Hyperbaric oxygen preconditioning improves postoperative cognitive dysfunction by reducing oxidant stress and inflammation

Postoperative cognitive dysfunction is a crucial public health issue that has been increasingly studied in efforts to reduce symptoms or prevent its occurrence. However, effective advances remain lacking. Hyperbaric oxygen preconditioning has proved to protect vital organs, such as the heart, liver, and brain. Recently, it has been introduced and widely studied in the prevention of postoperative cognitive dysfunction, with promising results. However, the neuroprotective mechanisms underlying this phenomenon remain controversial. This review summarizes and highlights the definition and application of hyperbaric oxygen preconditioning, the perniciousness and pathogenetic mechanism underlying postoperative cognitive dysfunction, and the effects that hyperbaric oxygen preconditioning has on postoperative cognitive dysfunction. Finally, we conclude that hyperbaric oxygen preconditioning is an effective and feasible method to prevent, alleviate, and improve postoperative cognitive dysfunction, and that its mechanism of action is very complex, involving the stimulation of endogenous antioxidant and anti-inflammation defense systems.

Significance of oxidative stress and antioxidant capacity tests as biomarkers of premature ovarian insufficiency: A case control study

BACKGROUND Premature ovarian insufficiency(POI)is a condition that causes secondary amenorrhea owing to ovarian hypofunction at an early stage.Early follicular depletion results in intractable infertility,thereby considerably reducing the quality of life of females.Given the continuum in weakened ovarian function,progressing from incipient ovarian failure(IOF)to transitional ovarian failure and further to POI,it is necessary to develop biomarkers for predicting POI.The oxidative stress states in IOF and POI were comprehensively evaluated via oxidative stress[diacron-reactive oxygen metabolites(d-ROMs)]test and anti-oxidant capacity[biological antioxidant potential(BAP)].METHODS Females presenting with secondary amenorrhea over 4 mo and a follicle stimulating hormone level of>40 mIU/mL were categorized into the POI group.Females presenting with a normal menstrual cycle and a follicle stimulating hormone level of>10.2 mIU/mL were categorized into the IOF group.Healthy females without ovarian hypofunction were categorized into the control group.Among females aged<40 years who visited our hospital from January 2021 to June 2022,we recruited 11 patients into both POI and IOF groups.For the potential antioxidant capacity,the relative oxidative stress index(BAP/d-ROMs×100)was calculated,and the oxidative stress defense system was comprehensively evaluated.RESULTS d-ROMs were significantly higher in the POI and IOF groups than in the control group,(478.2±58.7 U.CARR,434.5±60.6 U.CARR,and 341.1±35.1 U.CARR,respectively)(U.CARR is equivalent to 0.08 mg/dL of hydrogen peroxide).However,no significant difference was found between the POI and IOF groups.Regarding BAP,no significant difference was found between the control,IOF,and POI groups(2078.5±157.4μmol/L,2116.2±240.2μmol/L,and 2029.0±186.4μmol/L,respectively).The oxidative stress index was significantly higher in the POI and IOF groups than in the control group(23.7±3.3,20.7±3.6,and 16.5±2.1,respectively).However,no significant difference was found between the POI and IOF groups.CONCLUSION High levels of oxidative stress suggest that evaluating the oxidative stress state may be a useful indicator for the early detection of POI.

Acquired sensorineural hearing loss,oxidative stress,and microRNAs

Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-fa ctorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registe red clinical trials known to the senior author we re also assessed.A total of 222studies were thus identified.After excluding duplicates,editorials,retra ctions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferato r-activated receptor gamma coactivator-1-alpha(SIRT1/P GC-1α),SIRT1p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adve rse apoptotic effect,which was inhibited by resve ratrol and a myocardial inhibitorassociated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

Diabetes mellitus and glymphatic dysfunction:Roles for oxidative stress,mitochondria,circadian rhythm,artificial intelligence,and imaging

Diabetes mellitus(DM)is a debilitating disorder that impacts all systems of the body and has been increasing in prevalence throughout the globe.DM represents a significant clinical challenge to care for individuals and prevent the onset of chronic disability and ultimately death.Underlying cellular mechanisms for the onset and development of DM are multi-factorial in origin and involve pathways associated with the production of reactive oxygen species and the generation of oxidative stress as well as the dysfunction of mitochondrial cellular organelles,programmed cell death,and circadian rhythm impairments.These pathways can ultimately involve failure in the glymphatic pathway of the brain that is linked to circadian rhythms disorders during the loss of metabolic homeostasis.New studies incorporate a number of promising techniques to examine patients with metabolic disorders that can include machine learning and artificial intelligence pathways to potentially predict the onset of metabolic dysfunction.

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

Research on Oxidative Stress Induced by Tenuazonic Acid from Alternaria augustiovoide and Changes in Antioxidant Enzyme Activities in Leaves of Echinochloa crus-galli

[Objective] The aim of the study was to determine whether phytotoxicity of TeA against Echinochloa crus-galli leaves was correlated with oxidative stress caused by generation of reactive oxygen and the changes of antioxidant enzymes activity.[Method] The changes of malondialdehyde（MDA）content,hydrogen peroxide（H2O2）,and activities of superoxide dismutase（SOD）,glutathione reductase（GR）and catalase（CAT）were studied by leaf segment method in vitro.[Result] After the treatment of 500 μmol/L TeA,the content of MDA and H2O2 increased by 247.86% and 67.00%,respectively,indicating that the accumulation of MDA and H2O2 in E.crus-galli leaves was due to the reactive oxygen burst induced by TeA.TeA induced a significant increase in activities of SOD,GR and CAT.At 500 μmol/L TeA,activities of SOD,GR and CAT increased more than one fold compared with the control.[Conclusion] TeA could not only cause oxidative stress in leaves of E.crus-galli through the induction of reactive oxygen,but also induce the increasing of antioxidant enzyme activity.

Programmed cell death, antioxidant response and oxidative stress in wheat f lag leaves induced by chemical hybridization agent SQ-1

Male sterility induced by a chemical hybridization agent （CHA） is an important tool for utilizing crop heterosis. Leaves, especially the flag leaves, as CHA initial recipients play a decisive role in inducing male sterility. To investigate effects of different treatment times of CHA-SQ-1 used, morphological, biochemical and physiological responses of wheat flag leaves were detected in thistudy. CHA induced programmed cell death （PCD） as shown in terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling （TUNEL） and DNA laddering analysis. In the early phase, CHA-SQ-1 trig- gered organelle changes arid PCD in wheat leaves accompanied by excess production of reactive oxygen species （O2- and H202） and down-regulation of the activities of superoxide dismutase （SOD）, catalase （CAT） and guaiacol peroxidase （POD）. Meanwhile, leaf cell DNAs showed ladder-like patterns on agarose gel, indicating that CHA-SQ-1 led to the activation of the responsible endonuclease. The oxidative stress assays showed that lipid peroxidation was strongly activated and photosynthesis was obviously inhibited in SQ-l-induced leaves. However, CHA contents in wheat leaves gradually reduced along with the time CHA-SQ-1 applied. Young flags returned to an oxidative/antioxidative balance and ultimately developed into mature green leaves. These results provide explanation of the relations between PCD and anther abortion and practical application of CHA for hybrid breeding.

Exogenous Selenium Mitigates Salt Stress in Soybean by Improving Growth,Physiology,Glutathione Homeostasis and Antioxidant Defense

The mechanism of selenium(Se)-induced salt tolerance was studied in moderately sensitive soybean(Glycine max L.)plants.To execute this view,soybean plants were imposed with salt stress(EC 6 dS m^(−1))applying NaCl.In other treatments,Se(0,25,50 and 75μM Na_(2)SeO_(4))was sprayed as co-application with that level of salt stress.Plant height,stem diameter,leaf area,SPAD value decreased noticeably under salt stress.Altered proline(Pro)level,together with decreased leaf relative water content(RWC)was observed in salt-affected plants.Salt stress resulted in brutal oxidative damage and increased the content of H_(2)O_(2),MDA level and electrolyte leakage.Exogenous Se spray alleviated oxidative damage through boosting up the antioxidant defense system by increasing the activity of antioxidant enzymes such as catalase(CAT),peroxidase(POD)and glutathione reductase(GR),as well as by improving non-enzymatic antioxidants like glutathione(GSH)and GSH/glutathione disulfide(GSSG).The upregulated antioxidant defense system,restored Pro and leaf RWC,higher SPAD value conferred better growth and development in Se-sprayed salt-affected soybean plants which altogether put forth for the progressive yield contributing parameters and finally,seed yield.Among different doses of Se,soybean plants sprayed with 50μM Na_(2)SeO_(4)showed better salt tolerance.

Antioxidant enriched enteral nutrition and oxidative stress after major gastrointestinal tract surgery

AIM: To investigate the effects of an enteral supple-ment containing antioxidants on circulating levels of antioxidants and indicators of oxidative stress after major gastrointestinal surgery.METHODS: Twenty-one patients undergoing major upper gastrointestinal tract surgery were randomised in a single centre, open label study on the effect of postoperative enteral nutrition supplementedwith antioxidants. The effect on circulating levels of antioxidants and indicators of oxidative stress, such as F2-isoprostane, was studied. RESULTS: The antioxidant enteral supplement showed no adverse effects and was well tolerated. After surgery a decrease in the circulating levels of antioxidant parameters was observed. Only selenium and glutamine levels were restored to pre-operative values one week after surgery. F2-isoprostane increased in the first three postoperative days only in the antioxidant supplemented group. Lipopolysaccharide binding protein (LBP) levels decreased faster in the antioxidant group after surgery.CONCLUSION: Despite lower antioxidant levels there was no increase in the circulating markers of oxidative stress on the first day after major abdominal surgery. The rise in F2-isoprostane in patients receiving the antioxidant supplement may be related to the conversion of antioxidants to oxidants which raises questions on antioxidant supplementation. Module AOX restored the postoperative decrease in selenium levels. The rapid decrease in LBP levels in the antioxidant group suggests a possible protective effect on gut wall integrity. Further studies are needed on the role of oxidative stress on outcome and the use of antioxidants in patients undergoing major abdominal surgery.

Thyme oil and thymol abrogate doxorubicin-induced nephrotoxicity and cardiotoxicity in Wistar rats via repression of oxidative stress and enhancement of antioxidant defense mechanisms

This study aimed to assess the preventive effects of thyme oil and thymol on doxorubicin(DOX)-induced renotoxicity,cardiotoxicity,and oxidative stress in Wistar rats.Thyme oil was subjected to GC-MS analysis,which indicated that thymol was the major constituent representing 33.896%.Rats intraperitoneally injected with DOX at a dose of 2 mg/kg b.w./one per week for 7 weeks were co-treated with thyme oil and its major constituent,thymol,at doses 250 and 100 mg/kg b.w./every other day,respectively,by oral gavage for the same period.Thyme oil and thymol markedly ameliorated the raised levels of serum urea,uric acid,and creatinine in DOX-administered rats.They also reduced the elevated activities of serum CK-MB and LDH.Thyme oil was more effective than thymol in decreasing the elevated serum creatinine level and serum CK-MB activity in DOX-administered rats,thereby reflecting its more potent effect on kidney and heart functions.Lipid peroxidation significantly decreased while GSH level and GST and GPx activities significantly increased in kidney and heart of DOX-administered rats treated with thyme oil and thymol.The DOX-induced perturbed kidney histological changes including congestion of glomerulus tuft,inflammatory cells infiltration,protein cast in lumina of the renal tubule,and thickening of the parietal layer of Bowman’s capsule were remarkably ameliorated as a result of treatment with thyme oil and thymol;thyme oil was more effective.In addition,DOX-induced deleterious heart histological alterations,including intramuscular infiltration of inflammatory cells,focal necrosis of cardiac myocytes,and edema,were remarkably reduced by treatment with thyme oil and thymol.Thus,it can be concluded that DOX could induce marked toxicity in kidney and heart,and the treatment with thyme oil or thymol produced potential improvement of kidney and heart function and histological integrity via repression of oxidative stress and enhancement of antioxidant defense mechanisms.

Effect of astragaloside IV and salvianolic acid B on antioxidant stress and vascular endothelial protection in the treatment of atherosclerosis based on metabonomics

Vascular endothelial cells and oxidation reduction system play an important role in the pathogenesis of atherosclerosis(AS).If these conditions are disordered,it will inevitably lead to plaque formation and even rupture.Astragaloside IV(AsIV)and salvianolic acid B(Sal B)are the main active ingredients of Astragalus membranaceus and Salvia miltiorrhiza,respectively,and found to ameliorate vascular endothelial dysfunction and protect against oxidative stress in recent studies.However,it is still unknown if the combination of AsIV and Sal B(AsIV+Sal B)can inhibit the development of plaque through amplifying the protective effect of vascular endothelial cells and anti-oxidative stress effect.To clarify the role of AsIV+Sal B in AS,we observed the efficacy of each group(Control,Model,AsIV,Sal B,and AsIV+Sal B)by biomolecular assays,such as observing the pathological morphology of the aorta by oil red O staining,evaluating the level of oxidative stress and endothelial cells in the serum by the Elisa test,and analyzing the changes of all small molecule metabolites in liver tissue by UPLC-QTOF-MS.Results showed that AsIV,Sal B and AsIV+Sal B decreased the deposition of lipid in the arterial wall,so as to exert the effect of anti-oxidant stress and vascular endothelial protection,where the inhibitory effect of AsIV+Sal B was the most obvious.Metabonomics analysis showed that Sal B regulated the metabolic pathways of arginine and proline.AsIV regulated glycerol metabolism and saturated fatty acid biosynthesis metabolism.AsIV+Sal B is mainly related to the regulation of the citrate cycle(TCA cycle),alanine,aspartic acid,and glutamate metabolism,cysteine,and methionine metabolism.Succinic acid and methionine are synergistic metabolites that exert an enhancing effect when AsIV and Sal B were used in combination.In conclusion,we demonstrated that AsIV acompanied with Sal B can be successfully used for anti-oxidative stress and vascular endothelial protection of AS,and succinic acid and methionine are the synergistic metabolites.

Effects of Barium Stress in Brassica juncea and Cakile maritima:The Indicator Role of Some Antioxidant Enzymes and Secondary Metabolites

Soil contamination by toxic trace metal elements,like barium(Ba),may stimulate various undesirable changes in the metabolic activity of plants.The plant responses are fast and with,direct or indirect,generation of reactive oxygen species(ROS).To cope with the stress imposed by the ROS production,plants developed a dual cellular system composed of enzymatic and non-enzymatic players that convert ROS,and their by-products,into stable nontoxic molecules.To assess the Ba stress response of two Brassicaceae species(Brassica juncea,a glycophyte,and Cakile maritime,a halophyte),plants were exposure to different Ba concentrations(0,100,200,300 and 500µM).The plants response was evaluated through their morphology and development,the determination of plant leaves antioxidant enzymatic activities and by the production of plants secondary metabolites.Results indicated that the two Brassicaceae species have the ability to survive in an environment containing Ba(even at 500µM).The biomass production of C.maritima was slightly affected whereas an increase in biomass B.juncea was noticed.The stress imposed by Ba activated the antioxidant defense system in the two species,noticed by the changes in the leaves activity of catalase(CAT),ascorbate peroxidase(APX)and guaicol peroxidase(GPX),and of the secondary metabolites,through the production of total phenols and flavonoids.The enzymatic response was not similar within the two plant species:CAT and APX seem to have a more important role against the oxidative stress in C.maritima while in B.juncea is GPX.Overall,total phenols and flavonoids production was more significant in the plants aerial part than in the roots,of the both species.Although the two Brassicaceae species response was different,in both plants catalytic and non-catalytic transformation of ROS occurs,and both were able to overcome the Ba toxicity and prevent the cell damage.

Oxidative stress and antioxidants in diabetes mellitus

Numerous studies have implicated oxidative stress in the development of complications of diabetes.During hyperglycemia,production of oxidant agents such as reactive oxygen species and reactive nitrogen species increases.This process,along with a decrease in the activity of antioxidant enzymes,induces oxidative stress in the body.This redox imbalance causes damage to vital biomolecules such as proteins,lipids and DNA and results in the generation of harmful products for the body.Mechanisms associated with the creation of oxidative stress conditions and subsequently complications of diabetes are explained through several pathways such as flux through the polyol pathway,intracellular production of advanced glycation end products precursors,protein kinase-C activation,and increased activities of the hexosamine pathway.On the other hand,the study of polymorphism in the antioxidant enzymes genes indicates that some of the gene polymorphisms reduce the antioxidant power of the enzymes.This article aims to review various studies to demonstrate the effect of oxidative stress on the pathogenesis of diabetes and the positive role of antioxidants on diabetic complications.

Oxidative Stress and Role of Natural Plant Derived Antioxidants in Animal Reproduction

The experimental knowledge on the role of oxidative stress,and beneficial and detrimental effects of plant derived antioxidants in male and female animal reproduction are reviewed in this article.Free radical-induced oxidative stress in animal reproduction causes great loss to livestock industry.Antioxidant therapy has been implicated to be effective in preventing diseases resulted from oxidative stress.Considering the advantages of lower side effects of natural antioxidants than those of synthetic antioxidants,plants or their extracts have been extensively utilized in animals.Although many advances have been gained on application of plant derived antioxidants in alleviating oxidative stress,debatable issues still exist.Because many opposite effects were observed even using plant extracts containing similar bioactive substances in the same animal species.Therefore,plant derived antioxidants,like free radicals,are ＂double-edged swords＂ in animal reproduction,representing that they may exhibit beneficial or detrimental effects in animal reproduction,including spermatogenesis,semen functions,estrous cycles,ovulation,ovary functions,endometrium,embryo development,and pregnancy.Besides dose-dependent manner as an explanation of plant extracts＇ dual function,future studies are needed to investigate the mechanism of double-edged actions of plant derived antioxidants in different animal reproduction systems.

Biochanin-A attenuates high-fat diet and streptozotocin-induced hyperlipidemia and oxidative stress in rats by improving antioxidant status and lipid metabolic markers

Objective:To determine how biochanin-A(BCA)affects high-fat diet and streptozotocin-induced pathological changes in lipid metabolism and antioxidant status in diabetic rats.Methods:Diabetic rats were orally administered BCA(10 mg/kg body weight)for 30 days to investigate its effects on lipid profiles and oxidative stress markers in the liver and kidney.In addition,the mRNA expression of antioxidant and lipid metabolism enzymes in the liver was examined.Results:BCA attenuated hyperlipidemia by regulating mRNA expressions of HMG-CoA reductase,fatty acid synthase,carnitine palmitoyl transferase,and acetyl-CoA carboxylase.Additionally,BCA reduced high-fat diet and streptozotocin-induced oxidative stress by suppressing lipid peroxidation,improving superoxide dismutase,catalase,and glutathione peroxidase levels,and upregulating mRNA expressions of these enzymes.Conclusions:BCA may be a promising nutraceutical for the treatment of dyslipidemia and oxidative stress associated with diabetes.

Relationship between antioxidant capacity and oxidative stress in children with acute hepatitis A

AIM： To investigate in children with acute hepatitis A. According to our knowledge, there are no data about the blood levels of malondialdehyde （MDA, an indicator of oxidative stress） and nonenzymic antioxidants in children with acute hepatitis A. METHODS： Whole blood MDA and reduced glutathione （GSH）, serum β-carotene, retinol, vitamin E and vitamin C levels were studied in 19 （10 females, 9 males） children with acute hepatitis A and in 29 （β females, 16 males） healthy control subjects. RESULTS： There was a statistically significant difference between patients and controls for all parameters （P 〈 0.05）. Lipid peroxidation marker MDA was significantly elevated （P 〈 0.001）, while antioxidants β-carotene, retinol and GSH were significantly decreased （all P 〈 0.001） in patients compared to healthy subjects. In addition, o-tocopherol and ascorbic acid levels were significantly lower in patients when compared to age and sex matched controls （P 〈 0.05, P 〈 0.01, respectively）. CONCLUSION： Our study shows that hepatitis A virus induces oxidative stress in childern with hepatitis A. This finding could be taken into consideration to improve the therapeutic approach in acute hepatitis A.

Antioxidant efficiency of lycopene on oxidative stress-induced damage in bovine spermatozoa

Background： Lycopene（LYC） is a natural carotenoid with powerful reactive oxygen species（ROS） scavenging activities. The aim of this study was to investigate if lycopene has the ability to reverse ROS-mediated alterations to the motility, viability and intracellular antioxidant profile of bovine spermatozoa subjected to ferrous ascorbate（Fe AA）. Spermatozoa were washed out of fresh bovine semen, suspended in 2.9 % sodium citrate and subjected to LYC treatment（0.25, 0.5, 1 or 2 mmol/L） in the presence or absence of Fe AA（150 μmol/L Fe SO4 and 750 μmol/L ascorbic acid） during a 6 h in vitro culture. Spermatozoa motion characteristics were assessed using the Sperm Vision？computer-aided sperm analysis（CASA） system. Cell viability was examined with the metabolic activity（MTT） assay,ROS generation was quantified via luminometry and the nitroblue-tetrazolium（NBT） test was applied to quantify the intracellular superoxide formation. Cell lysates were prepared at the end of the in vitro culture to investigate the intracellular activity of superoxide dismutase（SOD）, catalase（CAT）, glutathione peroxidase（GPx） as well as the concentrations of glutathione（GSH） and malondialdehyde（MDA）.Results： FeA A treatment led to a reduced spermatozoa motility（P 〈 0.001）, viability（P 〈 0.001） and a decline of the antioxidant capacity of spermatozoa（P 〈 0.001） but increased the ROS generation（P 〈 0.001）, superoxide production（P 〈 0.001） and lipid peroxidation（P 〈 0.001）. LYC administration resulted in a preservation of the spermatozoa motion parameters（P 〈 0.001）, mitochondrial activity（P 〈 0.001） and antioxidant characteristics（P 〈 0.001 with respect to SOD;P 〈 0.01 in relation to CAT; P 〈 0.05 as for GPx and GSH） with a concentration range of 1 and 2 mmol/L LYC revealed to be the most effective.Conclusions： Our results suggest that LYC exhibits significant ROS-scavenging and antioxidant properties which may prevent spermatozoa alterations caused by oxidative stress, and preserve the functionality of male reproductive cells.

Effects of astaxanthin on antioxidant parameters in ARPE-19 cells on oxidative stress model

AIM: To observe the protective effect of astaxanthin(AST) against hydroquinone(HQ) mediated cell death in the apoptotic cascade and evaluate intracellular Ca2+ release, caspase-3, and-9 activation, reactive oxygen species(ROS) production in ARPE-19 cells.METHODS: We cultured ARPE-19 cells in special mediums and performed MTT tests to determine protective effect of AST, before exposing the cells to HQ in an incubator. We analyzed intracellular Ca2+ release experiments, mitochondrial membrane depolarization, glutathione(GSH), glutathione peroxidase(GSH-Px) and ROS experiments, and apoptosis assay.RESULTS: ROS production ranges depend on the amount of cell death. We computed the correlation between ROS ranges and cell death by 20,70-dichlorofluorescein fluorescence, and Ca2+ levels by Fura-2-AM. HQ-induced cell death found out to rise ranges of caspase-3 and-9, and mitochondrial depolarization. These three steps were delayed by AST management.CONCLUSION: ARPE-19 cells are avoided from HQinduced ROS production and caspase-3 and-9 activation by AST. AST may limit the range of caspase synthesis, Ca2+ release and excess production of ROS with antiapoptotic effect. This study proposes a new therapeutic approach for the treatment of age-related macular degeneration.

Activation of the wnt/β-catenin/CYP1B1 pathway alleviates oxidative stress and protects the blood-brain barrier under cerebral ischemia/reperfusion conditions

Accumulating evidence suggests that oxidative stress and the Wnt/β-catenin pathway participate in stroke-induced disruption of the blood-brain barrier.However,the potential links between them following ischemic stroke remain largely unknown.The present study found that cerebral ischemia leads to oxidative stress and repression of the Wnt/β-catenin pathway.Meanwhile,Wnt/β-catenin pathway activation by the pharmacological inhibito r,TWS119,relieved oxidative stress,increased the levels of cytochrome P4501B1(CYP1B1)and tight junction-associated proteins(zonula occludens-1[ZO-1],occludin and claudin-5),as well as brain microvascular density in cerebral ischemia rats.Moreove r,rat brain microvascular endothelial cells that underwent oxygen glucose deprivation/reoxygenation displayed intense oxidative stress,suppression of the Wnt/β-catenin pathway,aggravated cell apoptosis,downregulated CYP1B1and tight junction protein levels,and inhibited cell prolife ration and migration.Overexpression ofβ-catenin or knockdown ofβ-catenin and CYP1B1 genes in rat brain mic rovascular endothelial cells at least partly ameliorated or exacerbated these effects,respectively.In addition,small interfering RNA-mediatedβ-catenin silencing decreased CYP1B1 expression,whereas CYP1B1 knoc kdown did not change the levels of glycogen synthase kinase 3β,Wnt-3a,andβ-catenin proteins in rat brain microvascular endothelial cells after oxygen glucose deprivatio n/reoxygenation.Thus,the data suggest that CYP1B1 can be regulated by Wnt/β-catenin signaling,and activation of the Wnt/β-catenin/CYP1B1 pathway contributes to alleviation of oxidative stress,increased tight junction levels,and protection of the blood-brain barrier against ischemia/hypoxia-induced injury.

Biochanin A attenuates spinal cord injury in rats during early stages by inhibiting oxidative stress and inflammasome activation

Previous studies have shown that Biochanin A,a flavonoid compound with estrogenic effects,can serve as a neuroprotective agent in the context of cerebral ischemia/reperfusion injury;howeve r,its effect on spinal cord injury is still unclea r. In this study,a rat model of spinal cord injury was established using the heavy o bject impact method,and the rats were then treated with Biochanin A(40 mg/kg) via intrape ritoneal injection for 14 consecutive days.The res ults showed that Biochanin A effectively alleviated spinal cord neuronal injury and spinal co rd tissue injury,reduced inflammation and oxidative stress in spinal cord neuro ns,and reduced apoptosis and pyroptosis.In addition,Biochanin A inhibited the expression of inflammasome-related proteins(ASC,NLRP3,and GSDMD)and the Toll-like receptor 4/nuclear factor-κB pathway,activated the Nrf2/heme oxygenase 1 signaling pathway,and increased the expression of the autophagy markers LC3 Ⅱ,Beclin-1,and P62.Moreove r,the therapeutic effects of Biochanin A on early post-s pinal cord injury were similar to those of methylprednisolone.These findings suggest that Biochanin A protected neurons in the injured spinal cord through the Toll-like receptor 4/nuclear factor κB and Nrf2/heme oxygenase 1 signaling pathways.These findings suggest that Biochanin A can alleviate post-spinal cord injury at an early stage.