The changes of sclenium metabolism, glutathione peroxidase activity and lipid peroxidescontent in the tissues of rats suffering from 30% TBSA full thickness scalding were observed in thefirst 7 days after injury. It w...The changes of sclenium metabolism, glutathione peroxidase activity and lipid peroxidescontent in the tissues of rats suffering from 30% TBSA full thickness scalding were observed in thefirst 7 days after injury. It was found that selenium content in the rat tissues decreased remarkably af-ter injury, which in turn resulted in serious reduction of glutathione peroxidasc activity and significantincrease of lipid peroxides in the scrum, crythrocytcs and liver. However the muscular tissue showedno significant changes. These facts imply that after burn injury, the body is in a state of selenium deficiency, the lossof selenium might be responsible for the reduction of anti - peroxidation ability of glutathioneperoxidase, and conscqucntly there is an increase of lipid peroxides in the tissues. Only the musculartissue is insensitive to lipid peroxidation. It is believed that the reduction of anti-peroxidation abilityof glutathione peroxidasc after bum injury might be one of the main causes to intensify, the injury re-suiting from free radicals.展开更多
In the present paper, blood lipids peroxide(LPO) level and activities of glutathione peroxidase(GSH-Px) and superoxide dismutase(SOD) were investigated before and after combined treatment of acupuncture and moxibustio...In the present paper, blood lipids peroxide(LPO) level and activities of glutathione peroxidase(GSH-Px) and superoxide dismutase(SOD) were investigated before and after combined treatment of acupuncture and moxibustion and Chinese drugs in patients of vascular dementia(VD), and their results were compared with those in healthy persons with the similar ages to the patients. The results showed that the blood LPO level increased significantly, and the activities of SOD and GSH-Px reduced significantly in patients of VD as compared with those in the control group. Degrees of patient’s condition were related with amplitudes of the increase of LPO and the reduction of activities of GSHPx and SOD. Combined treatment of acupuncture and moxibustion and Chinese drugs could raise markedly activitles of blood GSH-Px and SOD, and lowered LPO level in the patients of VD, which are related to clinical therapeutic effects. It is considered that combination of acupuncture and moxibustion with Chinese drugs can increase the action of the antiperoxidative system in the patients of VD, exerting anti-peroxidative ability and clearing LPO and reducing the oxidative injury of the organism by oxygen free radical, which is one of mechanisms of combined treatment of acupuncture and moxibustion with Chinese drugs.展开更多
背景:有研究发现成骨细胞铁死亡可作为重要的发病机制诱导激素性股骨头坏死的发生与发展。随着祖国医学的发展,有学者发现某些中药单体、中药复方及中成药等可通过多种通路机制调控成骨细胞铁死亡,最终起到治疗激素性股骨头坏死的作用...背景:有研究发现成骨细胞铁死亡可作为重要的发病机制诱导激素性股骨头坏死的发生与发展。随着祖国医学的发展,有学者发现某些中药单体、中药复方及中成药等可通过多种通路机制调控成骨细胞铁死亡,最终起到治疗激素性股骨头坏死的作用。目的:探讨成骨细胞铁死亡与激素性股骨头坏死的关系及中草药调控成骨细胞铁死亡治疗激素性股骨头坏死的作用机制,为激素性股骨头坏死的诊治提供新的思路。方法:以“铁死亡,激素性股骨头坏死,成骨细胞,中草药,糖皮质激素,铁代谢,活性氧,谷胱甘肽过氧化物酶”为中文检索词,以“ferroptosis,Hormonal necrosis of the femoral head,osteoblast,Chinese herbal medicine,glucocorticoid,iron metabolism,ROS,GPX4”为英文检索词,检索中国知网、Pub Med、万方及维普数据库,筛选各数据库建库至2023年成骨细胞铁死亡与激素性股骨头坏死及中草药干预调控研究相关的文章,最终纳入74篇文献进行综述分析。结果与结论:(1)成骨细胞铁死亡在激素性股骨头坏死发病中起重要作用。(2)成骨细胞铁死亡的发生受到多种机制通路调控,如细胞内铁超载引起铁死亡;细胞发生脂质过氧化损伤细胞膜引起铁死亡;细胞膜上胱氨酸/谷氨酸逆向转运蛋白通过影响谷胱甘肽水平和谷胱甘肽过氧化物酶4活性,从而诱导铁死亡;细胞内发生芬顿反应产生大量活性氧引起铁死亡等。(3)中药单体淫羊藿苷等、中药复方青娥丸等及中成药补肾活血颗粒等均可通过调控成骨细胞铁死亡的发生,有助于防治激素性股骨头坏死。(4)目前关于成骨细胞铁死亡相关机制尚不明确,继续深入探明两者的作用机制,有望为临床治疗激素性股骨头坏死提供新选择。展开更多
Objective:To investigate the effects of different dietary fat and oils(differing in their degree of saturation and unsaturation)on lipid peroxidation in liver and blood of rats.Methods:The study was conducted on SO al...Objective:To investigate the effects of different dietary fat and oils(differing in their degree of saturation and unsaturation)on lipid peroxidation in liver and blood of rats.Methods:The study was conducted on SO albino rats that were randomly divided into 5 groups of 10 animals.The groups were fed on dietary butter(Group I),margarine(Croup II),olive oil(Group III),sunflower oil(Group IV)and com oil(Group V)for 7 weeks.After 12 h of diet removal,livers were excised and blood was collected to measure malondialdehyde(MDA)levels in the supernatant of liver homogenate and in blood.Blood superoxide dismutase activity(SOD),glutathione peroxidase activity(GPx),serum vitamin E and total antioxidant capacity(TAC)levels were also measured to determine the effects of fats and oils on lipid peroxidation.Results:The results indicated that no significant differences were observed in SOD activity,vitamin E and TAC levels between the five groups.However,there was significant decrease of GPx activity in groups IV and V when compared with otlier groups.The results indicated that feeding corn oil caused significant increases in liver and blood MDA levels as compared with other oils and fats.There were positive correlations between SOD and GPx,vitamin E and TAC as well as between GPx and TAC(r:0.743;P<0.001)and between blood MDA and liver MDA(r:0.897;P<0.00l).The results showed also negative correlations between blood MDA on one hand and SOD,GPx,vitamin E and TAC on the other hand.Conclusions:The results demonstrated that feeding oils rich in polyunsaturated fatly acids(PUFA)increases lipid peroxidation significantly and may raise the susceptibility of tissues to free radical oxidative damage.展开更多
We investigated the balance of free radicals in different tissues (liver, heart, brain and muscle) of rats in course of in vivo and in vitro processing by Macrovipera lebetina obtusa (MLO) and Montivipera raddei (MR) ...We investigated the balance of free radicals in different tissues (liver, heart, brain and muscle) of rats in course of in vivo and in vitro processing by Macrovipera lebetina obtusa (MLO) and Montivipera raddei (MR) snake venoms. Chemiluminescence (ChL) levels were examined in tissue assays after incubation (at 37 °C for a period of 10 min) with venom for in vitro experiments and in tissue assays isolated of 10 min after venom injection for in vivo experiments. The TBA-test was also performed to confirm the free radical expression. The activities of antioxidant enzymes (such as superoxide dismutase and glutathione peroxidase) in isolated tissues were detected by spectro-photometry. During the in vitro processing chemiluminescence levels of tissue homogenates significantly decreased, while in course of in vivo intoxication the level of ChL was elevated in brain and liver;lipid peroxidation also increased in brain tissue, but there was no significant balance change in other tissues;the activity of superoxide dismutase mainly correlated with changes of free radical balance during intoxication. On the contrary, the activity of glutathione peroxidase showed the reverse tendencies to change. We suggest that free radicals and their oxidative stresses may play a role in the early stage of intoxication causing the so-named “spreading-effect”, which is very characteristic for the venom of vipers.展开更多
The activities of superoxide dismutase (SOD). glutathione peroxidase (GSH-PX) in blood and the content of melondialdehyde (MDA) in plasma of 30 Fatients (male 17, female 13) with coronary artery disease (CAD) were de...The activities of superoxide dismutase (SOD). glutathione peroxidase (GSH-PX) in blood and the content of melondialdehyde (MDA) in plasma of 30 Fatients (male 17, female 13) with coronary artery disease (CAD) were determined in this study. It was shown that SOD and GSH-PX activities were decreased and the content of MDA was increased in the Patients comparative with the healthy controls (P<0.001). Vitamin C, the free radical scavenger, was then administered intravenously with a daily dose of 2g for 2 weeks. The activities of SOD and GSB-PX were significantly elevated (P<0.01, and P<0.05, respectively). and the level of MDA was obviously declined (P<0.01). Thus,the lipid peroxidation is involved in the pathogenesis of CAD,and vitamin C possessing some effects to ameliorate the lipid peroxidation damage could be helpful in the treatment of CAE.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
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
文摘The changes of sclenium metabolism, glutathione peroxidase activity and lipid peroxidescontent in the tissues of rats suffering from 30% TBSA full thickness scalding were observed in thefirst 7 days after injury. It was found that selenium content in the rat tissues decreased remarkably af-ter injury, which in turn resulted in serious reduction of glutathione peroxidasc activity and significantincrease of lipid peroxides in the scrum, crythrocytcs and liver. However the muscular tissue showedno significant changes. These facts imply that after burn injury, the body is in a state of selenium deficiency, the lossof selenium might be responsible for the reduction of anti - peroxidation ability of glutathioneperoxidase, and conscqucntly there is an increase of lipid peroxides in the tissues. Only the musculartissue is insensitive to lipid peroxidation. It is believed that the reduction of anti-peroxidation abilityof glutathione peroxidasc after bum injury might be one of the main causes to intensify, the injury re-suiting from free radicals.
文摘In the present paper, blood lipids peroxide(LPO) level and activities of glutathione peroxidase(GSH-Px) and superoxide dismutase(SOD) were investigated before and after combined treatment of acupuncture and moxibustion and Chinese drugs in patients of vascular dementia(VD), and their results were compared with those in healthy persons with the similar ages to the patients. The results showed that the blood LPO level increased significantly, and the activities of SOD and GSH-Px reduced significantly in patients of VD as compared with those in the control group. Degrees of patient’s condition were related with amplitudes of the increase of LPO and the reduction of activities of GSHPx and SOD. Combined treatment of acupuncture and moxibustion and Chinese drugs could raise markedly activitles of blood GSH-Px and SOD, and lowered LPO level in the patients of VD, which are related to clinical therapeutic effects. It is considered that combination of acupuncture and moxibustion with Chinese drugs can increase the action of the antiperoxidative system in the patients of VD, exerting anti-peroxidative ability and clearing LPO and reducing the oxidative injury of the organism by oxygen free radical, which is one of mechanisms of combined treatment of acupuncture and moxibustion with Chinese drugs.
文摘背景:有研究发现成骨细胞铁死亡可作为重要的发病机制诱导激素性股骨头坏死的发生与发展。随着祖国医学的发展,有学者发现某些中药单体、中药复方及中成药等可通过多种通路机制调控成骨细胞铁死亡,最终起到治疗激素性股骨头坏死的作用。目的:探讨成骨细胞铁死亡与激素性股骨头坏死的关系及中草药调控成骨细胞铁死亡治疗激素性股骨头坏死的作用机制,为激素性股骨头坏死的诊治提供新的思路。方法:以“铁死亡,激素性股骨头坏死,成骨细胞,中草药,糖皮质激素,铁代谢,活性氧,谷胱甘肽过氧化物酶”为中文检索词,以“ferroptosis,Hormonal necrosis of the femoral head,osteoblast,Chinese herbal medicine,glucocorticoid,iron metabolism,ROS,GPX4”为英文检索词,检索中国知网、Pub Med、万方及维普数据库,筛选各数据库建库至2023年成骨细胞铁死亡与激素性股骨头坏死及中草药干预调控研究相关的文章,最终纳入74篇文献进行综述分析。结果与结论:(1)成骨细胞铁死亡在激素性股骨头坏死发病中起重要作用。(2)成骨细胞铁死亡的发生受到多种机制通路调控,如细胞内铁超载引起铁死亡;细胞发生脂质过氧化损伤细胞膜引起铁死亡;细胞膜上胱氨酸/谷氨酸逆向转运蛋白通过影响谷胱甘肽水平和谷胱甘肽过氧化物酶4活性,从而诱导铁死亡;细胞内发生芬顿反应产生大量活性氧引起铁死亡等。(3)中药单体淫羊藿苷等、中药复方青娥丸等及中成药补肾活血颗粒等均可通过调控成骨细胞铁死亡的发生,有助于防治激素性股骨头坏死。(4)目前关于成骨细胞铁死亡相关机制尚不明确,继续深入探明两者的作用机制,有望为临床治疗激素性股骨头坏死提供新选择。
基金Supported by Qassum University,Kingdom of Saudi Arabia(Grant No.559)
文摘Objective:To investigate the effects of different dietary fat and oils(differing in their degree of saturation and unsaturation)on lipid peroxidation in liver and blood of rats.Methods:The study was conducted on SO albino rats that were randomly divided into 5 groups of 10 animals.The groups were fed on dietary butter(Group I),margarine(Croup II),olive oil(Group III),sunflower oil(Group IV)and com oil(Group V)for 7 weeks.After 12 h of diet removal,livers were excised and blood was collected to measure malondialdehyde(MDA)levels in the supernatant of liver homogenate and in blood.Blood superoxide dismutase activity(SOD),glutathione peroxidase activity(GPx),serum vitamin E and total antioxidant capacity(TAC)levels were also measured to determine the effects of fats and oils on lipid peroxidation.Results:The results indicated that no significant differences were observed in SOD activity,vitamin E and TAC levels between the five groups.However,there was significant decrease of GPx activity in groups IV and V when compared with otlier groups.The results indicated that feeding corn oil caused significant increases in liver and blood MDA levels as compared with other oils and fats.There were positive correlations between SOD and GPx,vitamin E and TAC as well as between GPx and TAC(r:0.743;P<0.001)and between blood MDA and liver MDA(r:0.897;P<0.00l).The results showed also negative correlations between blood MDA on one hand and SOD,GPx,vitamin E and TAC on the other hand.Conclusions:The results demonstrated that feeding oils rich in polyunsaturated fatly acids(PUFA)increases lipid peroxidation significantly and may raise the susceptibility of tissues to free radical oxidative damage.
文摘We investigated the balance of free radicals in different tissues (liver, heart, brain and muscle) of rats in course of in vivo and in vitro processing by Macrovipera lebetina obtusa (MLO) and Montivipera raddei (MR) snake venoms. Chemiluminescence (ChL) levels were examined in tissue assays after incubation (at 37 °C for a period of 10 min) with venom for in vitro experiments and in tissue assays isolated of 10 min after venom injection for in vivo experiments. The TBA-test was also performed to confirm the free radical expression. The activities of antioxidant enzymes (such as superoxide dismutase and glutathione peroxidase) in isolated tissues were detected by spectro-photometry. During the in vitro processing chemiluminescence levels of tissue homogenates significantly decreased, while in course of in vivo intoxication the level of ChL was elevated in brain and liver;lipid peroxidation also increased in brain tissue, but there was no significant balance change in other tissues;the activity of superoxide dismutase mainly correlated with changes of free radical balance during intoxication. On the contrary, the activity of glutathione peroxidase showed the reverse tendencies to change. We suggest that free radicals and their oxidative stresses may play a role in the early stage of intoxication causing the so-named “spreading-effect”, which is very characteristic for the venom of vipers.
文摘The activities of superoxide dismutase (SOD). glutathione peroxidase (GSH-PX) in blood and the content of melondialdehyde (MDA) in plasma of 30 Fatients (male 17, female 13) with coronary artery disease (CAD) were determined in this study. It was shown that SOD and GSH-PX activities were decreased and the content of MDA was increased in the Patients comparative with the healthy controls (P<0.001). Vitamin C, the free radical scavenger, was then administered intravenously with a daily dose of 2g for 2 weeks. The activities of SOD and GSB-PX were significantly elevated (P<0.01, and P<0.05, respectively). and the level of MDA was obviously declined (P<0.01). Thus,the lipid peroxidation is involved in the pathogenesis of CAD,and vitamin C possessing some effects to ameliorate the lipid peroxidation damage could be helpful in the treatment of CAE.
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.
