This study evaluated the mechanisms of 5-fluorouracil (5-FU) induced intestinal damage by investi-gating the lipid peroxide (LPO) level, myeloperoxidase (MPO) activity and disaccharidase activity in rats.Group Ⅰ anim...This study evaluated the mechanisms of 5-fluorouracil (5-FU) induced intestinal damage by investi-gating the lipid peroxide (LPO) level, myeloperoxidase (MPO) activity and disaccharidase activity in rats.Group Ⅰ animals (n=6) were sacrificed and served as a normal control group. Group Ⅱ animaIes (n= 24 )were given a single intraperitoneal injection of 5-FU (150 mg/kg) and every 8 rats were sacrificed on day1,3 and 5 after injection respectively. Results: LPO concentration in blood and intestinal mucosa was sig-nificantly higher in the group Ⅱ than in the group Ⅰ on day 1 and 3 (P<0. 05) MPO activity was signif-icantly higher in the group I than in the group Ⅰ at different times (P<0. 01 ). Lactase activity on day 5(P<0. 01); sucrase activity (P<0. 01 and P<0. 05 respectiviely) and maltase activity (P<0. 01 ) on day3 and 5, were significantly lower in the group than in the group l. Conclusion: The results indicatethat neutrophil infiltration may be involved in 5-FU-induced lipid peroxidative damage of the small intes-tine which was reflected by the decreased disaccharidases activities.展开更多
As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities ...As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.展开更多
Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease...Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease and cancer.Lipid-based reactive oxygen species(ROS),particularly lipid hydroperoxides in the cellular membrane can lead to membrane disruption and cell death mediated by ferroptosis.There are three necessary stages involving in the process of lipid peroxidation regulation in ferroptosis,including the synthesis of membrane phospholipids,initiation of lipid peroxidation and clearance of lipid peroxides.In this review,we summarized the molecular modulation mechanisms of lipid peroxidation in ferroptosis from the above three stages,as well as various ferroptosis modulators targeting lipid peroxidation,including commonly used products,natural bioactive compounds and selenocompounds.Collectively,these findings suggest the vital role of lipid peroxidation in ferroptosis,and targeting lipid peroxidation in ferroptosis is potential to treat ferroptosis-associated diseases.展开更多
Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,L...Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,Lao B,and Qiu YY.In this article,we added the correct citations of images.展开更多
BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attentio...BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.展开更多
Objective: To study the intervention effects of Jianpi Liqi Huoxue Decoction (健脾理气活血汤, JLHD) on lipid peroxidative liver injury induced by alcohol. Methods: The rat alcoholic model of liver disease (ALD) ...Objective: To study the intervention effects of Jianpi Liqi Huoxue Decoction (健脾理气活血汤, JLHD) on lipid peroxidative liver injury induced by alcohol. Methods: The rat alcoholic model of liver disease (ALD) induced by Lieber-DeCarli liquid diet was established. Thirty-two male SD rats were randomly divided into 4 groups : the normal group ( n = 5), the control group ( n = 9), the model group ( n = 9) and the JLHD group ( n =9). From the 4th week after modeling, the rats were given JLHD or distilled water by gastrogavage respectively, and the samples of blood and liver tissues were taken out from the rats for determination by the end of the 8th week. The hepatic pathological changes were observed with HE staining; the liver injury related indices, including activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, γ-glutamyl transpeptidase (γ-GT) activity and triglyceride (TG) content in liver tissues, as well as the lipid peroxidation related indices, including malonaldehyde (MDA) content and nitric oxide synthase (NOS) activity in liver tissue, serum Fe^2+ level, and the anti-peroxidation capacity related indices, including superoxide dismutase (SOD) activity, glutathion (GSH) content and reactive oxygen species (anti- ROS) activity in liver tissues were determined. Results: ( 1 ) There were obvious figures of fatty degeneration and inflammatory infiltration in liver tissues of the model group. As compared with the control group, in the model group, the activity of ALT and AST, and Fe^2+ content in serum, γ-GT and NOS activity, TG and MDA content in liver tissues were significantly higher ( P〈0. 01 ), while the activity of SOD, GSH and anti-ROS in liver tissues were significantly lower (P〈0.01). (2) The fatty degeneration and inflammatory infiltration of liver tissues in the JLHD group were significantly lessen as compared with those in the model group; and the abnormalities of all the indexes revealed in the model rats were restored to certain extent in the JLHD group, and especially significant were the levels of ALT activity, MDA content and Fe^2+ , which were nearly normal. Conclusion: JLHD has significant effects against alcoholic liver injury, the acting mechanism of which is likely to be related with its anti-lipid peroxidative effect.展开更多
Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,Parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders....Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,Parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders.Mitochondrial dysfunction,lipofuscin accumulation,autophagy disruption,and ferroptosis have been implicated as the critical pathomechanisms of lipid peroxidation and iron accumulation in these disorders.Currently,the connection between lipid peroxidation and iron accumulation and the initial cause or consequence in neurodegeneration processes is unclear.In this review,we have compiled the known mechanisms by which lipid peroxidation triggers iron accumulation and lipofuscin formation,and the effect of iron overload on lipid peroxidation and cellular function.The vicious cycle established between both pathological alterations may lead to the development of neurodegeneration.Therefore,the investigation of these mechanisms is essential for exploring therapeutic strategies to restrict neurodegeneration.In addition,we discuss the interplay between lipid peroxidation and iron accumulation in neurodegeneration,particularly in PLA2G6-associated neurodegeneration,a rare neurodegenerative disease with autosomal recessive inheritance,which belongs to the group of neurodegeneration with brain iron accumulation disorders.展开更多
This study aimed to analyze the effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7 S)and glycinin(11 S).Oxidation complexes were determined using the lipid peroxidat...This study aimed to analyze the effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7 S)and glycinin(11 S).Oxidation complexes were determined using the lipid peroxidation method.Functional properties were analyzed based on emulsifying and foaming properties.The potential allergenicity was evaluated by in vitro and in vivo methods.The results found that oxidation altered structures of the proteins and resulted in the formation of cross-linked protein polymers.The emulsion and foaming properties of the proteins were improved after oxidation.The IgE-binding capacity of 7 S and11 S reduced after oxidation.KU812 cell assays showed that both histamine and IL-4 release decreased after oxidation treatment.A mouse model showed that oxidation reduced the IgE,IgG,and IgG1 levels,as well as reduced histamine and mMCP-1 release in serum,which might suppress the allergic reaction.In conclusion,the lipid peroxidation treatment likely causes changes to the functional properties of soybean,decreasing the potential allergenicity of 7 S and 11 S.展开更多
Heavy metals have harmful effects on human health,and exposure to these metals has been increased by industrial and anthropogenic activities and modern industrialization.Heavy metals content of the liver tissues was d...Heavy metals have harmful effects on human health,and exposure to these metals has been increased by industrial and anthropogenic activities and modern industrialization.Heavy metals content of the liver tissues was determine d using Atomic Absorption Spectrophotometer method,while lipid peroxidation was carried out.Heavy metals analyzed include;lead(Pb),cadmium(Cd),zinc(Zn),Arsenic(As),and Mercury(Hg).The findings revealed that the heavy metal Zinc(Zn)has high concentrations in the muscles of the fish species,the concentration of this heavy metal Zinc is high in River Gindin Dorowa th a n in River Ibi and River Donga shows less concentration of this heavy metal though it’s above WHO permissible limits.Results revealed that only Zn and Cd were present in the muscle from the three rivers.Pb was found only in the liver from Gindin-Dorowa at the concentration of 0.017 mg/kg,which is not significant(P<0.05)when compared with other locations,while Hg and As were absent in all the muscle samples.The highest concentration of Zn was found in the muscle sample from Gindin-Dorowa(7.450 mg/kg)followed by Ibi(6.16 mg/kg)and the least being Donga(4.365 mg/kg)which are significantly(P<0.05)different from one another.However,there was no significant(P<0.05)difference among the Cd composition of muscle from Gindin-Dorowa(0.025 mg/kg),Donga(0.024 mg/kg)and Ibi(0.015 mg/kg),respectively.The TBA was found in the hepatic tissue sample from Gidin-Dorowa,which has the highest Zn,Cd and no Pb content,followed by Ibi and then the Donga sample.This suggests that there is a positive relationship between heavy metals and the effect of TBA on the hepatic tissues,justifying the fact that heavy metals affect the hepatic tissues of fish,while on the cerebral tissue.In conclusion,it revealed that there is a negative relation between heavy metals and the effect of TBA on the cerebral tissues to protect or save aquatic habitat s of fish quality and aquatic life.展开更多
Ferroptosis is a form of non-apoptotic programmed cell death,and its mechanisms mainly involve the accumulation of lipid peroxides,imbalance in the amino acid antioxidant system,and disordered iron metabolism.The prim...Ferroptosis is a form of non-apoptotic programmed cell death,and its mechanisms mainly involve the accumulation of lipid peroxides,imbalance in the amino acid antioxidant system,and disordered iron metabolism.The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum,and the progression of inflammatory diseases can trigger endoplasmic reticulum stress.Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival.Ferroptosis and endoplasmic reticulum stress may occur after ischemic stroke.However,there are few reports on the interactions of ferroptosis and endoplasmic reticulum stress with ischemic stroke.This review summarized the recent research on the relationships between ferroptosis and endoplasmic reticulum stress and ischemic stroke,aiming to provide a reference for developing treatments for ischemic stroke.展开更多
Regulated cell death is a genetically determined form of programmed cell death that commonly occurs during the development of living organisms.This process plays a crucial role in modulating homeostasis and is evoluti...Regulated cell death is a genetically determined form of programmed cell death that commonly occurs during the development of living organisms.This process plays a crucial role in modulating homeostasis and is evolutionarily conserved across a diverse range of living organisms.Ferroptosis is a classic regulatory mode of cell death.Extensive studies of regulatory cell death in Alzheimer’s disease have yielded increasing evidence that fe rroptosis is closely related to the occurrence,development,and prognosis of Alzheimer’s disease.This review summarizes the molecular mechanisms of ferroptosis and recent research advances in the role of ferro ptosis in Alzheimer’s disease.Our findings are expected to serve as a theoretical and experimental foundation for clinical research and targeted therapy for Alzheimer’s disease.展开更多
With indica ( Oryza sativa L.) hybrid Shanyou 63 as control, the hybrid rice varieties including Peiai 64S/E32, Peiai 64S/9311, X07S/Zihui 100, Guangyou 881 and japonica 9516 were used to study changes of chlorophyll ...With indica ( Oryza sativa L.) hybrid Shanyou 63 as control, the hybrid rice varieties including Peiai 64S/E32, Peiai 64S/9311, X07S/Zihui 100, Guangyou 881 and japonica 9516 were used to study changes of chlorophyll content, photosynthetic response to light intensity and temperature, chlorophyll fluorescence characteristics and membrane lipid peroxidation in their flag leaves at the late stage of development under natural conditions in Nanjing. The results were as follows:. primary photochemical efficiency of PS II ( F-v / F-m), quantum yield of linear electron transport of PS II (phi(PSII)), electron transfer rate (ETR) in these rice varieties decreased with their decrease of chlorophyll content during this period. This kind of impediment to energy conversion induced the transfer of excessive energy to the reducing side of PS I, hence the accumulation of O-2(radical anion) and peroxidation of membrane lipid, and resulting in the accumulation of malondialdehyde (MDA), that is the destroys of photosynthetic pigments and membranes and the consequent, premature senescence. This phenomenon is variable conspicuously in different rice varieties. Under natural condition in Nanjing, F-v/F-m, phi(PSII), ETR and quenching coefficient ( qP) in japonica 9516 tolerant to photooxidation decreased less and the conversion capacity of light energy was stable, premature senescence was unlikely, and consequently the seed-setting rate was higher. While F-v/F-m, phi(PSII), ETR and photochemical qP in Shanyou 63 sensitive to photooxidation decreased more and therefore premature senescence was easy to happen, thus the seed-setting rate and yield were all reduced. The tolerance to photooxidation and premature senescence in other hybrids derived from typical two line or three line crossing laid in the middle. From the rice breeding for super-high-yield, on the basis of the good plant-type of current rice, considering both hybrid vigor and the prevention premature senescence, it would be a notable strategy to use japonica maternal line or maternal. lines with some japonica genotype as the sterile lines in rice breeding.展开更多
[ Objective] The aim was to provide strategies for development of rare earth and control of environmental pollution. [ Method] Responses of membrane lipid peroxidation and endogenous hormones of soybean seedlings to U...[ Objective] The aim was to provide strategies for development of rare earth and control of environmental pollution. [ Method] Responses of membrane lipid peroxidation and endogenous hormones of soybean seedlings to UV-B radiation and rare earth were studied through hydroponics in laboratory. [ Result] The results showed that under irradiation of UV-B( T1-0.15 W/m^2 and T2-0.45 W/m^2), chlorophyll and indole-3-acetic acid(IAA) contents firstly decreased during the stress phase (1 -5 d) and then increased during the restoration phase (6 -9 d) while contents of malonadialdehyde(MDA) and abscisic acid(ABA) gradually increased during the imposition of UV-B radiation (1 -5 d) and subsequently decreased during recovery from UV-B stress (6 -9 d) . With adding of La (III) with the concentration of 20 mg · L^-1 , the decline/dse trend of chlorophyll, IAA, MDA and ABA contents was slowed down during the stress period while the rise/decline speed was accelerated during the recovery period. [ Conclusion] It suggests that the regulation of La ( III ) on membrane lipid peroxidation and endogenous hormones could increase chlorophyll and IAA contents, improve the metabolism of reactive oxygen species ( ROS), inhibit membrane lipid peroxidation, decrease the accumulation amount of ABA and alleviate injury of UV-B radiation to soybean seedlings. Further, the protective potential of La ( III ) was better under low UV-B radiation than under high one.展开更多
Relationships between fluorescence parameters and membrane lipid peroxidation in leaves of indica and japonica rice (Oryza sativa L.) during later growth stage were studied under chilling temperature and strong light ...Relationships between fluorescence parameters and membrane lipid peroxidation in leaves of indica and japonica rice (Oryza sativa L.) during later growth stage were studied under chilling temperature and strong light stress conditions. Results showed that D1 protein contents of PSⅡ in photosynthetic apparatus dropped, the generation of antheraxanthin (A) and zeaxanthin (Z) of xanthophyll cycle were inhibited partly, PSⅡ photochemical efficiency (F v/F m)and non-photochemical quenching (q N) were also decreased obviously. In addition, endogenous active oxygen scavenger—superoxide dismutase (SOD) reduced, superoxide anion radical (O -· 2) and malondialdehyde (MDA) accumulated, as a result, photooxidation of leaves occurred under chilling temperature and strong light stress conditions. Obvious differences in the changes of the above mentioned physiological parameters between indica and japonica rice were observed. Experiments in leaves treated with inhibitors under chilling temperature and strong light conditions showed that indica rice was more sensitive to chilling temperature with strong light and subjected to photooxidation more than japonica rice. Notable positive correlation between D1 protein contents and F v/F m or (A+Z)/(A+Z+V), and a marked negative correlation between F v/F m and MDA contents were obtained by regression analysis in indica and japonica rice during chilling temperature and strong light conditions. According to the facts mentioned above, it was inferred that PSⅡ photochemical efficiency(F v/F m) was the key index to forecast for the prediction of photooxidation under stress circumstances and the physiological basis were the synthetic capacity of D1 protein and the protection of xanthophyll cycle.展开更多
Previous studies have reported upregulation of heme oxygenase-1 in different central nervous system injury models.Heme oxygenase-1 plays a critical anti-inflammatory role and is essential for regulating cellular redox...Previous studies have reported upregulation of heme oxygenase-1 in different central nervous system injury models.Heme oxygenase-1 plays a critical anti-inflammatory role and is essential for regulating cellular redox homeostasis.Metformin is a classic drug used to treat type 2 diabetes that can inhibit ferroptosis.Previous studies have shown that,when used to treat cardiovascular and digestive system diseases,metformin can also upregulate heme oxygenase-1 expression.Therefore,we hypothesized that heme oxygenase-1 plays a significant role in mediating the beneficial effects of metformin on neuronal ferroptosis after spinal cord injury.To test this,we first performed a bioinformatics analysis based on the GEO database and found that heme oxygenase-1 was upregulated in the lesion of rats with spinal cord injury.Next,we confirmed this finding in a rat model of T9 spinal cord compression injury that exhibited spinal cord nerve cell ferroptosis.Continuous intraperitoneal injection of metformin for 14 days was found to both upregulate heme oxygenase-1 expression and reduce neuronal ferroptosis in rats with spinal cord injury.Subsequently,we used a lentivirus vector to knock down heme oxygenase-1 expression in the spinal cord,and found that this significantly reduced the effect of metformin on ferroptosis after spinal cord injury.Taken together,these findings suggest that metformin inhibits neuronal ferroptosis after spinal cord injury,and that this effect is partially dependent on upregulation of heme oxygenase-1.展开更多
The effects of water─soluble components isolated from Salvia miltiorrhiza on oxygen free radical prodction and lipid peroxidation were estimated. Five components(10 μmol/L)were shown to inhibit superoxide anion gen...The effects of water─soluble components isolated from Salvia miltiorrhiza on oxygen free radical prodction and lipid peroxidation were estimated. Five components(10 μmol/L)were shown to inhibit superoxide anion generation by xanthine─xanthine oxidase system. It was also demonstrated that six components( 100 μmol/L) prevented H_2O_2─induced hemolysis and MDA fonnation in mouse erythrocytes.The effects of Sal A, Sal B, Sal C and Ros A were dose dependent. In Langendorff rat heart, pretreatment with Sal A 20μmol/L significantly prevented MDA production induced by 30 min reoxygenation after 45 min anoxia.The results indicated that there were also other potent antioxidant componentts in Salvia milliorrhiza besides Dphl and Pal. The protection of Sal A against myocardial anoxiareoxygenation inury may be mainly ascribed to its oxygen free radical scavenging activity.展开更多
[Objective] Effects of different concentrations of nitric oxide on membrane lipid peroxidation of wheat induced by enhanced UV-B radiation were researched,sodium nitroprusside (SNP) was selected as an exogenous nitr...[Objective] Effects of different concentrations of nitric oxide on membrane lipid peroxidation of wheat induced by enhanced UV-B radiation were researched,sodium nitroprusside (SNP) was selected as an exogenous nitric oxide(NO)donor.[Method] There are 3 groups including CK,UV treatment group (B),B+SNP treatment group,0,1,2,3,4 d sampling after treatment respectively,and physiological and biochemical indexes of MDA content and CAT,POD,SOD and so on were determined,repeated 3 times,and statistical analyzed.[Result] The results showed that,after the enhanced UV-B radiation,activity of the catalase (CAT),superoxide dismutase (SOD) and of the guaiacol peroxidase (POD) all reduced apparently,and the concentration of malondialdehyde (MDA) increased obviously,leading to oxidative damage in wheat seedlings.Impose different concentrations of SNP after UV-B radiation,may mitigate oxidative damage of wheat seedling from different degrees,which was in agreement with the effect of making the concentration of MDA decrease and the activity of the CAT,SOD and POD all increased.The mitigation role of 0.01 mol/L SNP was more obvious for roots' oxidative damage,while 0.1 mmol/L SNP is more effective for oxidative damage of leaves.[Conclusion] Exogenous NO donor SNP had obvious relieve effects on oxidative damage of wheat seedlings caused by UV-B radiation,which can enhance adaptive capacity of plants to adversity stress.展开更多
[ Objective] The aim of this study was to discuss the effect of antioxidants and lipid peroxidation from pea crops of plateau. [ Method] SOD enzyme liquid from pea crops of plateau was extracted by means of protein co...[ Objective] The aim of this study was to discuss the effect of antioxidants and lipid peroxidation from pea crops of plateau. [ Method] SOD enzyme liquid from pea crops of plateau was extracted by means of protein concentration assay, enzyme activity assay and antioxidant activity determination by DPPH method, peroxide activity inhibition of in vitro tissues from mice by homogenate MDA colorimetry method and lipid peroxidation assay of in vitro tissues. [ Result ] IC50 of the crude enzyme liquid extracted from pea on DPPH was 55.16 mg/L, while the scavenging rate of the crude enzyme liquid was lower than that of ascorbic acid, tea polyphenol and citric acid with the same concentration. The synergistic effect was found in ascorbic acid and crude enzyme liquid, but the synergism of ascorbic acid was better than that of citric acid. IC50 of SOD enzyme liquid extracted from pea on DPPH was 11.1 mg/L, which was better than that of tea polyphenol and closely similar to that of ascorbic acid. SOD enzyme liquid extracted from pea had an inhibitory effect on MDA production from in vitro tissues such as liver, kidney and heart, especially for a significantly inhibitory effect on MDA from liver in vitro. When the concentration was 0.25 mg/ml, the inhibition rate reached 78.3%, and then the inhibition rate increased little with the concentration incresas, while its effect on heart and kidney were inferior. [ Conclusion] SOD crude enzyme liquid and SOD enzyme liquid extracted from pea all have certain DPPH scavenging capacity, while SOD enzyme liquid extracted from pea has an inhibitory effect on lipid peroxidation.展开更多
Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxid...Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.展开更多
Interfering with the ferroptosis pathway is a new strategy for the treatment of spinal cord injury.Fibroblast growth factor 21 can inhibit ferro ptosis and promote neurofunctional recovery,while heme oxygenase-1 is a ...Interfering with the ferroptosis pathway is a new strategy for the treatment of spinal cord injury.Fibroblast growth factor 21 can inhibit ferro ptosis and promote neurofunctional recovery,while heme oxygenase-1 is a regulator of iron and reactive oxygen species homeostasis.The relationship between heme oxygenase-1and ferroptosis remains controve rsial.In this study,we used a spinal co rd injury rat model to show that the levels of fibroblast growth factor 21 in spinal co rd tissue decreased after spinal cord injury.In addition,there was a significant aggravation of ferroptosis and a rapid increase in heme oxygenase-1 expression after spinal cord injury.Furthe r,heme oxygenase-1 aggravated fe rroptosis after spinal cord injury,while fibroblast growth factor 21 inhibited fe rroptosis by downregulating heme oxygenase-1.Thus,the activation of fibroblast growth factor 21 may provide a potential treatment for spinal co rd injury.These findings could provide a new potential mechanistic explanation for fibroblast growth factor 21 in the treatment of spinal cord injury.展开更多
文摘This study evaluated the mechanisms of 5-fluorouracil (5-FU) induced intestinal damage by investi-gating the lipid peroxide (LPO) level, myeloperoxidase (MPO) activity and disaccharidase activity in rats.Group Ⅰ animals (n=6) were sacrificed and served as a normal control group. Group Ⅱ animaIes (n= 24 )were given a single intraperitoneal injection of 5-FU (150 mg/kg) and every 8 rats were sacrificed on day1,3 and 5 after injection respectively. Results: LPO concentration in blood and intestinal mucosa was sig-nificantly higher in the group Ⅱ than in the group Ⅰ on day 1 and 3 (P<0. 05) MPO activity was signif-icantly higher in the group I than in the group Ⅰ at different times (P<0. 01 ). Lactase activity on day 5(P<0. 01); sucrase activity (P<0. 01 and P<0. 05 respectiviely) and maltase activity (P<0. 01 ) on day3 and 5, were significantly lower in the group than in the group l. Conclusion: The results indicatethat neutrophil infiltration may be involved in 5-FU-induced lipid peroxidative damage of the small intes-tine which was reflected by the decreased disaccharidases activities.
文摘As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.
基金supported by Jiangxi Provincial Natural Science Foundation(20224BAB216091,20224ACB205014)Jiangxi Provincial Department of Education Science and Technology Plan Project(GJJ2200420).
文摘Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease and cancer.Lipid-based reactive oxygen species(ROS),particularly lipid hydroperoxides in the cellular membrane can lead to membrane disruption and cell death mediated by ferroptosis.There are three necessary stages involving in the process of lipid peroxidation regulation in ferroptosis,including the synthesis of membrane phospholipids,initiation of lipid peroxidation and clearance of lipid peroxides.In this review,we summarized the molecular modulation mechanisms of lipid peroxidation in ferroptosis from the above three stages,as well as various ferroptosis modulators targeting lipid peroxidation,including commonly used products,natural bioactive compounds and selenocompounds.Collectively,these findings suggest the vital role of lipid peroxidation in ferroptosis,and targeting lipid peroxidation in ferroptosis is potential to treat ferroptosis-associated diseases.
文摘Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,Lao B,and Qiu YY.In this article,we added the correct citations of images.
文摘BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.
基金Supported by the National Natural Science Foundation of China (No.30371818) and Project of Key Subject Construction of Shanghai (Y0302)
文摘Objective: To study the intervention effects of Jianpi Liqi Huoxue Decoction (健脾理气活血汤, JLHD) on lipid peroxidative liver injury induced by alcohol. Methods: The rat alcoholic model of liver disease (ALD) induced by Lieber-DeCarli liquid diet was established. Thirty-two male SD rats were randomly divided into 4 groups : the normal group ( n = 5), the control group ( n = 9), the model group ( n = 9) and the JLHD group ( n =9). From the 4th week after modeling, the rats were given JLHD or distilled water by gastrogavage respectively, and the samples of blood and liver tissues were taken out from the rats for determination by the end of the 8th week. The hepatic pathological changes were observed with HE staining; the liver injury related indices, including activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, γ-glutamyl transpeptidase (γ-GT) activity and triglyceride (TG) content in liver tissues, as well as the lipid peroxidation related indices, including malonaldehyde (MDA) content and nitric oxide synthase (NOS) activity in liver tissue, serum Fe^2+ level, and the anti-peroxidation capacity related indices, including superoxide dismutase (SOD) activity, glutathion (GSH) content and reactive oxygen species (anti- ROS) activity in liver tissues were determined. Results: ( 1 ) There were obvious figures of fatty degeneration and inflammatory infiltration in liver tissues of the model group. As compared with the control group, in the model group, the activity of ALT and AST, and Fe^2+ content in serum, γ-GT and NOS activity, TG and MDA content in liver tissues were significantly higher ( P〈0. 01 ), while the activity of SOD, GSH and anti-ROS in liver tissues were significantly lower (P〈0.01). (2) The fatty degeneration and inflammatory infiltration of liver tissues in the JLHD group were significantly lessen as compared with those in the model group; and the abnormalities of all the indexes revealed in the model rats were restored to certain extent in the JLHD group, and especially significant were the levels of ALT activity, MDA content and Fe^2+ , which were nearly normal. Conclusion: JLHD has significant effects against alcoholic liver injury, the acting mechanism of which is likely to be related with its anti-lipid peroxidative effect.
基金supported by FIS PI16/00786(2016)and FIS PI19/00377(2019)grantsthe Ministerio de Sanidad,Spain and the Fondo Europeo de Desarrollo Regional(FEDER Unión Europea)Spanish Ministry of Education,Culture and Sport.This activity has been co-financed by the European Regional Development Fund(ERDF)and by the Regional Ministry of Economic Transformation,Industry,Knowledge and Universities of the Junta de Andalucía,within the framework of the ERDF Andalusia operational program 2014-2020 Thematic objective“01-Reinforcement of research,technological development and innovation”through the reference research project CTS-5725 and PY18-850(to JASA).
文摘Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,Parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders.Mitochondrial dysfunction,lipofuscin accumulation,autophagy disruption,and ferroptosis have been implicated as the critical pathomechanisms of lipid peroxidation and iron accumulation in these disorders.Currently,the connection between lipid peroxidation and iron accumulation and the initial cause or consequence in neurodegeneration processes is unclear.In this review,we have compiled the known mechanisms by which lipid peroxidation triggers iron accumulation and lipofuscin formation,and the effect of iron overload on lipid peroxidation and cellular function.The vicious cycle established between both pathological alterations may lead to the development of neurodegeneration.Therefore,the investigation of these mechanisms is essential for exploring therapeutic strategies to restrict neurodegeneration.In addition,we discuss the interplay between lipid peroxidation and iron accumulation in neurodegeneration,particularly in PLA2G6-associated neurodegeneration,a rare neurodegenerative disease with autosomal recessive inheritance,which belongs to the group of neurodegeneration with brain iron accumulation disorders.
基金supported in part by the National Natural Science Foundation of China(32172311)Key-Area Research and Development Program of Guangdong Province(2019B020213001)+1 种基金Guangdong Basic and Applied Basic Research Foundation(2021A1515012413)the support from the Instrumental Analysis Center of Shenzhen University(Xili Campus)。
文摘This study aimed to analyze the effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7 S)and glycinin(11 S).Oxidation complexes were determined using the lipid peroxidation method.Functional properties were analyzed based on emulsifying and foaming properties.The potential allergenicity was evaluated by in vitro and in vivo methods.The results found that oxidation altered structures of the proteins and resulted in the formation of cross-linked protein polymers.The emulsion and foaming properties of the proteins were improved after oxidation.The IgE-binding capacity of 7 S and11 S reduced after oxidation.KU812 cell assays showed that both histamine and IL-4 release decreased after oxidation treatment.A mouse model showed that oxidation reduced the IgE,IgG,and IgG1 levels,as well as reduced histamine and mMCP-1 release in serum,which might suppress the allergic reaction.In conclusion,the lipid peroxidation treatment likely causes changes to the functional properties of soybean,decreasing the potential allergenicity of 7 S and 11 S.
文摘Heavy metals have harmful effects on human health,and exposure to these metals has been increased by industrial and anthropogenic activities and modern industrialization.Heavy metals content of the liver tissues was determine d using Atomic Absorption Spectrophotometer method,while lipid peroxidation was carried out.Heavy metals analyzed include;lead(Pb),cadmium(Cd),zinc(Zn),Arsenic(As),and Mercury(Hg).The findings revealed that the heavy metal Zinc(Zn)has high concentrations in the muscles of the fish species,the concentration of this heavy metal Zinc is high in River Gindin Dorowa th a n in River Ibi and River Donga shows less concentration of this heavy metal though it’s above WHO permissible limits.Results revealed that only Zn and Cd were present in the muscle from the three rivers.Pb was found only in the liver from Gindin-Dorowa at the concentration of 0.017 mg/kg,which is not significant(P<0.05)when compared with other locations,while Hg and As were absent in all the muscle samples.The highest concentration of Zn was found in the muscle sample from Gindin-Dorowa(7.450 mg/kg)followed by Ibi(6.16 mg/kg)and the least being Donga(4.365 mg/kg)which are significantly(P<0.05)different from one another.However,there was no significant(P<0.05)difference among the Cd composition of muscle from Gindin-Dorowa(0.025 mg/kg),Donga(0.024 mg/kg)and Ibi(0.015 mg/kg),respectively.The TBA was found in the hepatic tissue sample from Gidin-Dorowa,which has the highest Zn,Cd and no Pb content,followed by Ibi and then the Donga sample.This suggests that there is a positive relationship between heavy metals and the effect of TBA on the hepatic tissues,justifying the fact that heavy metals affect the hepatic tissues of fish,while on the cerebral tissue.In conclusion,it revealed that there is a negative relation between heavy metals and the effect of TBA on the cerebral tissues to protect or save aquatic habitat s of fish quality and aquatic life.
基金supported by the National Natural Science Foundation of China,Nos.82071339 and 82271370(both to LG).
文摘Ferroptosis is a form of non-apoptotic programmed cell death,and its mechanisms mainly involve the accumulation of lipid peroxides,imbalance in the amino acid antioxidant system,and disordered iron metabolism.The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum,and the progression of inflammatory diseases can trigger endoplasmic reticulum stress.Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival.Ferroptosis and endoplasmic reticulum stress may occur after ischemic stroke.However,there are few reports on the interactions of ferroptosis and endoplasmic reticulum stress with ischemic stroke.This review summarized the recent research on the relationships between ferroptosis and endoplasmic reticulum stress and ischemic stroke,aiming to provide a reference for developing treatments for ischemic stroke.
基金supported by the National Natural Science Foundation of China,No.81501106(to CF)Fund of Taishan Scholar Project(to CF)+1 种基金the Natural Science Foundation of Shandong Province,No.ZR2020QH106(to YH)the Medical and Health Science and Technology Development Plan of Shandong Province,No.202203010799(to QS)。
文摘Regulated cell death is a genetically determined form of programmed cell death that commonly occurs during the development of living organisms.This process plays a crucial role in modulating homeostasis and is evolutionarily conserved across a diverse range of living organisms.Ferroptosis is a classic regulatory mode of cell death.Extensive studies of regulatory cell death in Alzheimer’s disease have yielded increasing evidence that fe rroptosis is closely related to the occurrence,development,and prognosis of Alzheimer’s disease.This review summarizes the molecular mechanisms of ferroptosis and recent research advances in the role of ferro ptosis in Alzheimer’s disease.Our findings are expected to serve as a theoretical and experimental foundation for clinical research and targeted therapy for Alzheimer’s disease.
文摘With indica ( Oryza sativa L.) hybrid Shanyou 63 as control, the hybrid rice varieties including Peiai 64S/E32, Peiai 64S/9311, X07S/Zihui 100, Guangyou 881 and japonica 9516 were used to study changes of chlorophyll content, photosynthetic response to light intensity and temperature, chlorophyll fluorescence characteristics and membrane lipid peroxidation in their flag leaves at the late stage of development under natural conditions in Nanjing. The results were as follows:. primary photochemical efficiency of PS II ( F-v / F-m), quantum yield of linear electron transport of PS II (phi(PSII)), electron transfer rate (ETR) in these rice varieties decreased with their decrease of chlorophyll content during this period. This kind of impediment to energy conversion induced the transfer of excessive energy to the reducing side of PS I, hence the accumulation of O-2(radical anion) and peroxidation of membrane lipid, and resulting in the accumulation of malondialdehyde (MDA), that is the destroys of photosynthetic pigments and membranes and the consequent, premature senescence. This phenomenon is variable conspicuously in different rice varieties. Under natural condition in Nanjing, F-v/F-m, phi(PSII), ETR and quenching coefficient ( qP) in japonica 9516 tolerant to photooxidation decreased less and the conversion capacity of light energy was stable, premature senescence was unlikely, and consequently the seed-setting rate was higher. While F-v/F-m, phi(PSII), ETR and photochemical qP in Shanyou 63 sensitive to photooxidation decreased more and therefore premature senescence was easy to happen, thus the seed-setting rate and yield were all reduced. The tolerance to photooxidation and premature senescence in other hybrids derived from typical two line or three line crossing laid in the middle. From the rice breeding for super-high-yield, on the basis of the good plant-type of current rice, considering both hybrid vigor and the prevention premature senescence, it would be a notable strategy to use japonica maternal line or maternal. lines with some japonica genotype as the sterile lines in rice breeding.
基金Supported by the Foundation of State Developing and ReformingCommittee(No.IFZ20051210)the National Natural Science Foundationof China(No.30570323,No.20471030)the Programsin Science and Technology of Nantong(No.DE2009006,No.S2009019)~~
文摘[ Objective] The aim was to provide strategies for development of rare earth and control of environmental pollution. [ Method] Responses of membrane lipid peroxidation and endogenous hormones of soybean seedlings to UV-B radiation and rare earth were studied through hydroponics in laboratory. [ Result] The results showed that under irradiation of UV-B( T1-0.15 W/m^2 and T2-0.45 W/m^2), chlorophyll and indole-3-acetic acid(IAA) contents firstly decreased during the stress phase (1 -5 d) and then increased during the restoration phase (6 -9 d) while contents of malonadialdehyde(MDA) and abscisic acid(ABA) gradually increased during the imposition of UV-B radiation (1 -5 d) and subsequently decreased during recovery from UV-B stress (6 -9 d) . With adding of La (III) with the concentration of 20 mg · L^-1 , the decline/dse trend of chlorophyll, IAA, MDA and ABA contents was slowed down during the stress period while the rise/decline speed was accelerated during the recovery period. [ Conclusion] It suggests that the regulation of La ( III ) on membrane lipid peroxidation and endogenous hormones could increase chlorophyll and IAA contents, improve the metabolism of reactive oxygen species ( ROS), inhibit membrane lipid peroxidation, decrease the accumulation amount of ABA and alleviate injury of UV-B radiation to soybean seedlings. Further, the protective potential of La ( III ) was better under low UV-B radiation than under high one.
文摘Relationships between fluorescence parameters and membrane lipid peroxidation in leaves of indica and japonica rice (Oryza sativa L.) during later growth stage were studied under chilling temperature and strong light stress conditions. Results showed that D1 protein contents of PSⅡ in photosynthetic apparatus dropped, the generation of antheraxanthin (A) and zeaxanthin (Z) of xanthophyll cycle were inhibited partly, PSⅡ photochemical efficiency (F v/F m)and non-photochemical quenching (q N) were also decreased obviously. In addition, endogenous active oxygen scavenger—superoxide dismutase (SOD) reduced, superoxide anion radical (O -· 2) and malondialdehyde (MDA) accumulated, as a result, photooxidation of leaves occurred under chilling temperature and strong light stress conditions. Obvious differences in the changes of the above mentioned physiological parameters between indica and japonica rice were observed. Experiments in leaves treated with inhibitors under chilling temperature and strong light conditions showed that indica rice was more sensitive to chilling temperature with strong light and subjected to photooxidation more than japonica rice. Notable positive correlation between D1 protein contents and F v/F m or (A+Z)/(A+Z+V), and a marked negative correlation between F v/F m and MDA contents were obtained by regression analysis in indica and japonica rice during chilling temperature and strong light conditions. According to the facts mentioned above, it was inferred that PSⅡ photochemical efficiency(F v/F m) was the key index to forecast for the prediction of photooxidation under stress circumstances and the physiological basis were the synthetic capacity of D1 protein and the protection of xanthophyll cycle.
文摘Previous studies have reported upregulation of heme oxygenase-1 in different central nervous system injury models.Heme oxygenase-1 plays a critical anti-inflammatory role and is essential for regulating cellular redox homeostasis.Metformin is a classic drug used to treat type 2 diabetes that can inhibit ferroptosis.Previous studies have shown that,when used to treat cardiovascular and digestive system diseases,metformin can also upregulate heme oxygenase-1 expression.Therefore,we hypothesized that heme oxygenase-1 plays a significant role in mediating the beneficial effects of metformin on neuronal ferroptosis after spinal cord injury.To test this,we first performed a bioinformatics analysis based on the GEO database and found that heme oxygenase-1 was upregulated in the lesion of rats with spinal cord injury.Next,we confirmed this finding in a rat model of T9 spinal cord compression injury that exhibited spinal cord nerve cell ferroptosis.Continuous intraperitoneal injection of metformin for 14 days was found to both upregulate heme oxygenase-1 expression and reduce neuronal ferroptosis in rats with spinal cord injury.Subsequently,we used a lentivirus vector to knock down heme oxygenase-1 expression in the spinal cord,and found that this significantly reduced the effect of metformin on ferroptosis after spinal cord injury.Taken together,these findings suggest that metformin inhibits neuronal ferroptosis after spinal cord injury,and that this effect is partially dependent on upregulation of heme oxygenase-1.
文摘The effects of water─soluble components isolated from Salvia miltiorrhiza on oxygen free radical prodction and lipid peroxidation were estimated. Five components(10 μmol/L)were shown to inhibit superoxide anion generation by xanthine─xanthine oxidase system. It was also demonstrated that six components( 100 μmol/L) prevented H_2O_2─induced hemolysis and MDA fonnation in mouse erythrocytes.The effects of Sal A, Sal B, Sal C and Ros A were dose dependent. In Langendorff rat heart, pretreatment with Sal A 20μmol/L significantly prevented MDA production induced by 30 min reoxygenation after 45 min anoxia.The results indicated that there were also other potent antioxidant componentts in Salvia milliorrhiza besides Dphl and Pal. The protection of Sal A against myocardial anoxiareoxygenation inury may be mainly ascribed to its oxygen free radical scavenging activity.
基金Supported by National Natural Science Foundation of China(No.30671061)Natural Science Foundation of Shanxi Province(No.2008011059-1 and No.20041101)~~
文摘[Objective] Effects of different concentrations of nitric oxide on membrane lipid peroxidation of wheat induced by enhanced UV-B radiation were researched,sodium nitroprusside (SNP) was selected as an exogenous nitric oxide(NO)donor.[Method] There are 3 groups including CK,UV treatment group (B),B+SNP treatment group,0,1,2,3,4 d sampling after treatment respectively,and physiological and biochemical indexes of MDA content and CAT,POD,SOD and so on were determined,repeated 3 times,and statistical analyzed.[Result] The results showed that,after the enhanced UV-B radiation,activity of the catalase (CAT),superoxide dismutase (SOD) and of the guaiacol peroxidase (POD) all reduced apparently,and the concentration of malondialdehyde (MDA) increased obviously,leading to oxidative damage in wheat seedlings.Impose different concentrations of SNP after UV-B radiation,may mitigate oxidative damage of wheat seedling from different degrees,which was in agreement with the effect of making the concentration of MDA decrease and the activity of the CAT,SOD and POD all increased.The mitigation role of 0.01 mol/L SNP was more obvious for roots' oxidative damage,while 0.1 mmol/L SNP is more effective for oxidative damage of leaves.[Conclusion] Exogenous NO donor SNP had obvious relieve effects on oxidative damage of wheat seedlings caused by UV-B radiation,which can enhance adaptive capacity of plants to adversity stress.
文摘[ Objective] The aim of this study was to discuss the effect of antioxidants and lipid peroxidation from pea crops of plateau. [ Method] SOD enzyme liquid from pea crops of plateau was extracted by means of protein concentration assay, enzyme activity assay and antioxidant activity determination by DPPH method, peroxide activity inhibition of in vitro tissues from mice by homogenate MDA colorimetry method and lipid peroxidation assay of in vitro tissues. [ Result ] IC50 of the crude enzyme liquid extracted from pea on DPPH was 55.16 mg/L, while the scavenging rate of the crude enzyme liquid was lower than that of ascorbic acid, tea polyphenol and citric acid with the same concentration. The synergistic effect was found in ascorbic acid and crude enzyme liquid, but the synergism of ascorbic acid was better than that of citric acid. IC50 of SOD enzyme liquid extracted from pea on DPPH was 11.1 mg/L, which was better than that of tea polyphenol and closely similar to that of ascorbic acid. SOD enzyme liquid extracted from pea had an inhibitory effect on MDA production from in vitro tissues such as liver, kidney and heart, especially for a significantly inhibitory effect on MDA from liver in vitro. When the concentration was 0.25 mg/ml, the inhibition rate reached 78.3%, and then the inhibition rate increased little with the concentration incresas, while its effect on heart and kidney were inferior. [ Conclusion] SOD crude enzyme liquid and SOD enzyme liquid extracted from pea all have certain DPPH scavenging capacity, while SOD enzyme liquid extracted from pea has an inhibitory effect on lipid peroxidation.
基金supported by the National Natural Science Foundation of China,No.82071442 (to LS)a grant from the Jilin Provincial Department of Finance,No.JLSWSRCZX2021-004 (to LS)。
文摘Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.
基金supported by grants from Jiangsu Commission of Health,No.Z2021086(to XL)Science and Technology Program of Suzhou,Nos.SYSD2020008(to XL),SKYD2022012(to XL)+1 种基金Suzhou Municipal Health Commission,No.KJXW2020058(to XL)Science and Technology Program of Zhangjiagang,No.ZKS2018(to XL)。
文摘Interfering with the ferroptosis pathway is a new strategy for the treatment of spinal cord injury.Fibroblast growth factor 21 can inhibit ferro ptosis and promote neurofunctional recovery,while heme oxygenase-1 is a regulator of iron and reactive oxygen species homeostasis.The relationship between heme oxygenase-1and ferroptosis remains controve rsial.In this study,we used a spinal co rd injury rat model to show that the levels of fibroblast growth factor 21 in spinal co rd tissue decreased after spinal cord injury.In addition,there was a significant aggravation of ferroptosis and a rapid increase in heme oxygenase-1 expression after spinal cord injury.Furthe r,heme oxygenase-1 aggravated fe rroptosis after spinal cord injury,while fibroblast growth factor 21 inhibited fe rroptosis by downregulating heme oxygenase-1.Thus,the activation of fibroblast growth factor 21 may provide a potential treatment for spinal co rd injury.These findings could provide a new potential mechanistic explanation for fibroblast growth factor 21 in the treatment of spinal cord injury.