期刊文献+
共找到4,675篇文章
< 1 2 234 >
每页显示 20 50 100
Anti-oxidative stress treatment and current clinical trials
1
作者 Chun-Ye Zhang Ming Yang 《World Journal of Hepatology》 2024年第2期294-299,共6页
Oxidative stress disturbs the balance between the production of reactive oxygen species(ROS)and the detoxification biological process.It plays an important role in the development and progression of many chronic disea... Oxidative stress disturbs the balance between the production of reactive oxygen species(ROS)and the detoxification biological process.It plays an important role in the development and progression of many chronic diseases.Upon exposure to oxidative stress or the inducers of ROS,the cellular nucleus undergoes some biological processes via different signaling pathways,such as stress adaption through the forkhead box O signaling pathway,inflammatory response through the IκB kinase/nuclear factor-κB signaling pathway,hypoxic response via the hypoxia-inducible factor/prolyl hydroxylase domain proteins pathway,DNA repair or apoptosis through the p53 signaling pathway,and antioxidant response through the Kelch-like ECH-associated protein 1/nuclear factor E2-related factor 2 signaling pathway.These processes are involved in many diseases.Therefore,oxidative stress has gained more attraction as a targeting process for disease treatment.Meanwhile,anti-oxidative stress agents have been widely explored in pre-clinical trials.However,only limited clinical trials are performed to evaluate the efficacy of anti-oxidative stress agents or antioxidants in diseases.In this letter,we further discuss the current clinical trials related to anti-oxidative stress treatment in different diseases.More pre-clinical studies and clinical trials are expected to use anti-oxidative stress strategies as disease treatment or dietary supplementation to improve disease treatment outcomes. 展开更多
关键词 anti-oxidative stress treatment Clinical trials DRUGS Dietary invention Reactive oxygen species
下载PDF
Treatment with β-sitosterol ameliorates the effects of cerebral ischemia/reperfusion injury by suppressing cholesterol overload, endoplasmic reticulum stress, and apoptosis 被引量:4
2
作者 Xiuling Tang Tao Yan +8 位作者 Saiying Wang Qingqing Liu Qi Yang Yongqiang Zhang Yujiao Li Yumei Wu Shuibing Liu Yulong Ma Le Yang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期642-649,共8页
β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unkno... β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unknown whetherβ-sitosterol treatment reduces the effects of ischemic stroke.Here we found that,in a mouse model of ischemic stroke induced by middle cerebral artery occlusion,β-sitosterol reduced the volume of cerebral infarction and brain edema,reduced neuronal apoptosis in brain tissue,and alleviated neurological dysfunction;moreover,β-sitosterol increased the activity of oxygen-and glucose-deprived cerebral cortex neurons and reduced apoptosis.Further investigation showed that the neuroprotective effects ofβ-sitosterol may be related to inhibition of endoplasmic reticulum stress caused by intracellular cholesterol accumulation after ischemic stroke.In addition,β-sitosterol showed high affinity for NPC1L1,a key transporter of cholesterol,and antagonized its activity.In conclusion,β-sitosterol may help treat ischemic stroke by inhibiting neuronal intracellular cholesterol overload/endoplasmic reticulum stress/apoptosis signaling pathways. 展开更多
关键词 APOPTOSIS blood-brain barrier Β-SITOSTEROL cerebral ischemia/reperfusion injury cholesterol overload cholesterol transport endoplasmic reticulum stress ischemic stroke molecular docking NPC1L1
下载PDF
Biochanin A attenuates spinal cord injury in rats during early stages by inhibiting oxidative stress and inflammasome activation 被引量:2
3
作者 Xigong Li Jing Fu +3 位作者 Ming Guan Haifei Shi Wenming Pan Xianfeng Lou 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2050-2056,共7页
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 ... 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. 展开更多
关键词 apoptosis AUTOPHAGY Biochanin A heme oxygenase 1 INFLAMMATION Nrf2 protein nuclear factor kappa-B oxidative stress spinal cord injury Toll-like receptor 4
下载PDF
Betulin protects against isoproterenol-induced myocardial injury by inhibiting NF-κB signaling and attenuating cardiac inflammation and oxidative stress in rats
4
作者 Hital Shah Tejal Gandhi 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2024年第6期236-244,共9页
Objective:To investigate the cardioprotective potential of betulin in isoproterenol(ISO)-induced myocardial injury in rats.Methods:Wistar rats were divided into five groups(n=10):normal,ISO,nebivolol 5 mg/kg,and betul... Objective:To investigate the cardioprotective potential of betulin in isoproterenol(ISO)-induced myocardial injury in rats.Methods:Wistar rats were divided into five groups(n=10):normal,ISO,nebivolol 5 mg/kg,and betulin(20&40 mg/kg).Nebivolol and betulin were administered orally for 29 days.ISO(85 mg/kg)was administered subcutaneously on day 27 and day 28 to induce myocardial injury.On day 29,blood was collected for determination of cardiac markers,and hemodynamic parameters were investigated.The levels of oxidative stress markers and the gene expressions of apoptotic markers and inflammatory mediators were evaluated.Moreover,2,3,5-triphenyltetrazolium chloride staining and histopathological analysis were also performed.Results:Betulin reduced the size of myocardial infarction,decreased elevated levels of cardiac enzymes,and maintained hemodynamic functions.It also inhibited ISO-induced upregulation of Bax,caspase-3,NF-κB,and IL-6,enhanced endogenous antioxidant enzymes,and reduced lipid peroxidation.Additionally,pretreatment with betulin alleviated myocardial ischemic damage,as reflected by reduced myonecrosis,edema,and inflammatory changes.Conclusions:Betulin exhibits strong cardioprotective activity against ISO-induced myocardial injury by anti-inflammatory,anti-apoptotic,and antioxidant activities. 展开更多
关键词 NF-ΚB ISOPROTERENOL BETULIN Myocardial injury Oxidative stress INFLAMMATION Apoptosis
下载PDF
Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention
5
作者 Ju Zheng Yixin Li +8 位作者 Ting Zhang Yanlin Fu Peiyan Long Xiao Gao Zhengwei Wang Zhizhong Guan Xiaolan Qi Wei Hong Yan Xiao 《Neural Regeneration Research》 SCIE CAS 2025年第5期1455-1466,共12页
Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cereb... Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains unclear.In this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury.We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced autophagy.Furthermore,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy.Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury.Findings from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury. 展开更多
关键词 APOPTOSIS ATF4 AUTOPHAGY C/EBP homologous protein cerebral ischemia/reperfusion injury EIF2Α endoplasmic reticulum stress PERK
下载PDF
Exosomes derived from microglia overexpressing miR-124-3p alleviate neuronal endoplasmic reticulum stress damage after repetitive mild traumatic brain injury
6
作者 Yan Wang Dai Li +12 位作者 Lan Zhang Zhenyu Yin Zhaoli Han Xintong Ge Meimei Li Jing Zhao Shishuang Zhang Yan Zuo Xiangyang Xiong Han Gao Qiang Liu Fanglian Chen Ping Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2010-2018,共9页
We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repet... We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repetitive mild traumatic brain injury remains unclear.In this study,we first used an HT22 scratch injury model to mimic traumatic brain injury,then co-cultured the HT22 cells with BV2 microglia expressing high levels of miR-124-3p.We found that exosomes containing high levels of miR-124-3p attenuated apoptosis and endoplasmic reticulum stress.Furthermore,luciferase reporter assay analysis confirmed that miR-124-3p bound specifically to the endoplasmic reticulum stress-related protein IRE1α,while an IRE1αfunctional salvage experiment confirmed that miR-124-3p targeted IRE1αand reduced its expression,thereby inhibiting endoplasmic reticulum stress in injured neurons.Finally,we delivered microglia-derived exosomes containing miR-124-3p intranasally to a mouse model of repetitive mild traumatic brain injury and found that endoplasmic reticulum stress and apoptosis levels in hippocampal neurons were significantly reduced.These findings suggest that,after repetitive mild traumatic brain injury,miR-124-3 can be transferred from microglia-derived exosomes to injured neurons,where it exerts a neuroprotective effect by inhibiting endoplasmic reticulum stress.Therefore,microglia-derived exosomes containing miR-124-3p may represent a novel therapeutic strategy for repetitive mild traumatic brain injury. 展开更多
关键词 apoptosis C/EBP homologous protein endoplasmic reticulum stress EXOSOME inositol-requiring enzyme MICROGLIA miR-124-3p neuron repetitive mild traumatic brain injury X-box binding protein 1
下载PDF
Inhibiting tau protein improves the recovery of spinal cord injury in rats by alleviating neuroinflammation and oxidative stress 被引量:9
7
作者 Guo-Liang Chen Kai Sun +5 位作者 Xi-Zhe Liu Kui-Leung Tong Zi-Juan Chen Lu Yu Ning-Ning Chen Shao-Yu Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第8期1834-1840,共7页
After spinal cord injury,the concentrations of total and hyperphosphorylated tau in cerebrospinal fluid increase,and levels of both correlate with injury severity.Tau inhibition is considered effective therapy for man... After spinal cord injury,the concentrations of total and hyperphosphorylated tau in cerebrospinal fluid increase,and levels of both correlate with injury severity.Tau inhibition is considered effective therapy for many central nervous system diseases,including traumatic brain injury and Alzheimer's disease.However,whether it can play a role in the treatment of spinal cord injury remains unclear.In this study,the therapeutic effects of tau inhibition were investigated in a rat model of transection spinal cord injury by injecting the rats with a lentivirus encoding tau siRNA that inhibits tau expression.We found that tau inhibition after spinal cord injury down-regulated the levels of inflammatory mediators,including tumor necrosis factor-α,interleukin-6 and interleukin-1β.It also led to a shift of activated microglial polarization from the M1 pro-inflammatory phenotype to the M2 anti-inflammatory phenotype,and reduced the amount of reactive oxygen species in the acute phase.Furthermore,the survival of residual neural cells around the injury epicenter,and neuronal and axonal regeneration were also markedly enhanced,which promoted locomotor recovery in the model rats.Collectively,our findings support the conclusion that tau inhibition can attenuate neuroinflammation,alleviate oxidative stress,protect residual cells,facilitate neurogenesis,and improve the functional recovery after spinal cord injury,and thus suggest that tau could be a good molecular target for spinal cord injury therapy. 展开更多
关键词 functional recovery MAPK pathway microglial polarization NEUROINFLAMMATION neuronal regeneration oxidative stress spinal cord injury TAU
下载PDF
Impact loading in female runners with single and multiple bone stress injuries during fresh and exerted conditions 被引量:1
8
作者 Kristin L.Popp Jereme Outerleys +7 位作者 Sarah Gehman Margaret Garrahan Sara Rudolph Elizabeth Loranger Kathryn E.Ackerman Adam S.Tenforde Mary L.Bouxsein Irene S.Davis 《Journal of Sport and Health Science》 SCIE CSCD 2023年第3期406-413,共8页
Background:Bone stress injuries(BSIs)are common in female runners,and recurrent BSI rates are high.Previous work suggests an association between higher impact loading during running and tibial BSI.However,it is unknow... Background:Bone stress injuries(BSIs)are common in female runners,and recurrent BSI rates are high.Previous work suggests an association between higher impact loading during running and tibial BSI.However,it is unknown whether impact loading and fatigue-related loading changes discriminate women with a history of multiple BSIs.This study compared impact variables at the beginning of a treadmill run to exertion andthe changes in those variables with exertion among female runners with no history of BSI as well as among those with a history of single or multiple BSIs.Methods:We enrolled 45 female runners(aged 18-40 years)for this cross-sectional study:having no history of diagnosed lower extremity BSI(N-BSI,n=14);a history of 1 lower extremity BSI(1-BSI,n=16);and diagnosed by imaging,or a history of multiple(>3)lower extremity BSIs(M-BSI,n=15).Participants completed a 5-km race speed run on an instrumented treadmill while wearing an Inertial Measurement Unit.The vertical average loading rate(VALR),vertical instantaneous loading rate(VILR),vertical stiffness during impact via instrumented treadmill,and tibial shock determined as the peak po sitive tibial acceleration via Inertial Measurement Unit were measured at the beginning and the end of the run.Results:There were no differences between groups in VALR,VILR,vertical stiffness,or tibial shock in a fresh or exerted condition.However,compared to N-BSI,women with M-BSI had greater increase with exertion in VALR(-1.8%vs.6.1%,p=0.01)and VILR(1.5%vs.4.8%,p=0.03).Similarly,compared to N-BSI,vertical stiffness increased more with exertion among women with M-BSI(-0.9%vs.7.3%,p=0.006)and 1-BSI(-0.9%vs.1.8%,p=0.05).Finally,compared to N-BSI,the increase in tibial shock from fresh to exerted condition was greater among women with M-BSI(0.9%vs.5.5%,p=0.03)and 1-BSI(0.9%vs.11.2%,p=0.02).Conclusion:Women with 1-BSI or M-BSIs experience greater exertion-related increases in impact loading than women with N-BSI.These observations imply that exertion-related changes in gait biomechanics may contribute to risk of BSI. 展开更多
关键词 BIOMECHANICS Bone stress injuries FATIGUE RUNNERS stress fracture
下载PDF
Hydralazine Promotes Central Nervous System Recovery after Spinal Cord Injury by Suppressing Oxidative Stress and Inflammation through Macrophage Regulation 被引量:1
9
作者 Xin QUAN Teng MA +4 位作者 Kai GUO Huan WANG Cai-yong YU Chu-chu QI Bao-qiang SONG 《Current Medical Science》 SCIE CAS 2023年第4期749-758,共10页
Objective:This study aims to investigate the effects of hydralazine on inflammation induced by spinal cord injury(SCI)in the central nervous system(CNS)and its mechanism in promoting the structural and functional reco... Objective:This study aims to investigate the effects of hydralazine on inflammation induced by spinal cord injury(SCI)in the central nervous system(CNS)and its mechanism in promoting the structural and functional recovery of the injured CNS.Methods:A compressive SCI mouse model was utilized for this investigation.Immunofluorescence and quantitative real-time polymerase chain reaction were employed to examine the levels of acrolein,acrolein-induced inflammation-related factors,and macrophages at the injury site and within the CNS.Western blotting was used to evaluate the activity of the phosphoinositide 3-kinase(PI3K)/AKT pathway to study macrophage regulation.The neuropathic pain and motor function recovery were evaluated by glutamic acid decarboxylase 65/67(GAD65/67),vesicular glutamate transporter 1(VGLUT1),paw withdrawal response,and Basso Mouse Scale score.Nissl staining and Luxol Fast Blue(LFB)staining were performed to investigate the structural recovery of the injured CNS.Results:Hydralazine downregulated the levels of acrolein,IL-1β,and TNF-αin the spinal cord.The downregulation of acrolein induced by hydralazine promoted the activation of the PI3K/AKT pathway,leading to M2 macrophage polarization,which protected neurons against SCI-induced inflammation.Additionally,hydralazine promoted the structural recovery of the injured spinal cord area.Mitigating inflammation and oxidative stress by hydralazine in the animal model alleviated neuropathic pain and altered neurotransmitter expression.Furthermore,hydralazine facilitated motor function recovery following SCI.Nissl staining and LFB staining indicated that hydralazine promoted the structural recovery of the injured CNS.Conclusion:Hydralazine,an acrolein scavenger,significantly mitigated SCI-induced inflammation and oxidative stress in vivo,modulated macrophage activation,and consequently promoted the structural and functional recovery of the injured CNS. 展开更多
关键词 spinal cord injury proinflammation oxidative stress MACROPHAGE acrolein scavenger
下载PDF
Reducing Dietary Cation-Anion Difference on Acid-Base Balance, Plasma Minerals Level and Anti-Oxidative Stress of Female Goats 被引量:3
10
作者 WU Wen-xuan YANG Yi +1 位作者 ZHANG Ji-kun LI Sheng-li 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2013年第9期1620-1628,共9页
Reducing dietary cation-anion difference (DCAD) has been proved an effective way to prevent milk fever in dairy cows. Based on the similar physiological gastro-intestinal tract anatomy and metabolic process between ... Reducing dietary cation-anion difference (DCAD) has been proved an effective way to prevent milk fever in dairy cows. Based on the similar physiological gastro-intestinal tract anatomy and metabolic process between female goats and dairy cows, this study was conducted to evaluate the effects of varying DCAD on fluid acid-base status, plasma minerals concentration and anti-oxidative stress capacity of female goats. Urinary pH, plasma Ca, P and Mg; and anti-oxidative stress indices of total superoxide dismutase (T-SOD), hydrogen peroxide (HzO2), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were determined to evaluate the effect. Forty-eight Guizhou black female goats ((15±1.9) mon of old, (22.3±3.75) kg of BW) were randomly allocated to 4 blocks of 12 goats each and were fed 1 of 4 diets differed in DCAD level (calculated as Na+K-C1-S, mEq kg-1 DM). Levels of DCAD were preliminarily designed to be control (+ 150 mEq kg^-1 DM, CON), high DCAD (+300 mEq kg^-1 DM, HD), low DCAD (0 mEq kg^-1 DM, LD) and negative DCAD (-150 mEq kg^-1 DM, ND), respectively. A commercial anionic salts (Animate) and sodium bicarbonate (NaHCO3) were supplemented to reduce and increase DCAD level, respectively. There was no difference in dry matter intake for 4 groups of goats. Urine pH was aggressively decreased (P〈0.0001) with reduced DCAD and there was a strong association between DCAD and urine pH (R2=0.793, P〈0.0001). Compared with CON and HD feeding of LD and ND resulted in greater (P〈0.05) plasma Ca concentration. Plasma P level was increased (P〈0.05) when anionic salts were supplemented. The DCAD alteration did not affected (P〉0.05) plasma Mg level. There was no significant (P〉0.05) difference in plasma GSH-Px activity and H202, but anionic salts supplementation in LD and ND significantly increased (P〈0.05) plasma T-SOD activity and tended to reduce MDA (P〈0.1) over HD and CON. Results from this study indicated that reducing DCAD could decrease urine pH and increase plasma Ca concentration of female goats. Additionally, reducing DCAD was helpful to enhance anti-oxidative stress capability of female goats. 展开更多
关键词 dietary cation-anion difference urine pH plasma calcium anti-oxidative stress female goats
下载PDF
Uridine diphosphate glucuronosyltransferase 1A1 prevents the progression of liver injury 被引量:1
11
作者 Jin-Lian Jiang Yi-Yang Zhou +8 位作者 Wei-Wei Zhong Lin-Yan Luo Si-Ying Liu Xiao-Yu Xie Mao-Yuan Mu Zhi-Gang Jiang Yuan Xue Jian Zhang Yi-Huai He 《World Journal of Gastroenterology》 SCIE CAS 2024年第9期1189-1212,共24页
BACKGROUND Uridine diphosphate glucuronosyltransferase 1A1(UGT1A1)plays a crucial role in metabolizing and detoxifying endogenous and exogenous substances.However,its contribution to the progression of liver damage re... BACKGROUND Uridine diphosphate glucuronosyltransferase 1A1(UGT1A1)plays a crucial role in metabolizing and detoxifying endogenous and exogenous substances.However,its contribution to the progression of liver damage remains unclear.AIM To determine the role and mechanism of UGT1A1 in liver damage progression.METHODS We investigated the relationship between UGT1A1 expression and liver injury through clinical research.Additionally,the impact and mechanism of UGT1A1 on the progression of liver injury was analyzed through a mouse model study.RESULTS Patients with UGT1A1 gene mutations showed varying degrees of liver damage,while patients with acute-onchronic liver failure(ACLF)exhibited relatively reduced levels of UGT1A1 protein in the liver as compared to patients with chronic hepatitis.This suggests that low UGT1A1 levels may be associated with the progression of liver damage.In mouse models of liver injury induced by carbon tetrachloride(CCl_(4))and concanavalin A(ConA),the hepatic levels of UGT1A1 protein were found to be increased.In mice with lipopolysaccharide or liver steatosis-mediated liver-injury progression,the hepatic protein levels of UGT1A1 were decreased,which is consistent with the observations in patients with ACLF.UGT1A1 knockout exacerbated CCl_(4)-and ConA-induced liver injury,hepatocyte apoptosis and necroptosis in mice,intensified hepatocyte endoplasmic reticulum(ER)stress and oxidative stress,and disrupted lipid metabolism.CONCLUSION UGT1A1 is upregulated as a compensatory response during liver injury,and interference with this upregulation process may worsen liver injury.UGT1A1 reduces ER stress,oxidative stress,and lipid metabolism disorder,thereby mitigating hepatocyte apoptosis and necroptosis. 展开更多
关键词 Uridine diphosphate glucuronosyltransferase 1A1 Liver injury progression Endoplasmic reticulum stress Oxidative stress Lipid metabolism disorders
下载PDF
Duodenal-jejunal bypass improves hypothalamic oxidative stress and inflammation in diabetic rats via glucagon-like peptide 1-mediated Nrf2/HO-1 signaling 被引量:1
12
作者 Huai-Jie Wang Li-Bin Zhang +4 位作者 Si-Peng Sun Qing-Tao Yan Zhi-Qin Gao Fang-Ming Fu Mei-Hua Qu 《World Journal of Diabetes》 SCIE 2024年第2期287-304,共18页
BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal je... BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal jejunal bypass(DJB)surgery significantly improves brain glucose metabolism in T2DM rats,the role and the metabolism of DJB in improving brain oxidative stress and inflammation condition in T2DM rats remain unclear.AIM To investigate the role and metabolism of DJB in improving hypothalamic oxidative stress and inflammation condition in T2DM rats.METHODS A T2DM rat model was induced via a high-glucose and high-fat diet,combined with a low-dose streptozotocin injection.T2DM rats were divided into DJB operation and Sham operation groups.DJB surgical intervention was carried out on T2DM rats.The differential expression of hypothalamic proteins was analyzed using quantitative proteomics analysis.Proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of T2DM rats were analyzed by flow cytometry,quantitative real-time PCR,Western blotting,and immunofluorescence.RESULTS Quantitative proteomics analysis showed significant differences in proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of rats with T2DM-DJB after DJB surgery,compared to the T2DM-Sham groups of rats.Oxidative stress-related proteins(glucagon-like peptide 1 receptor,Nrf2,and HO-1)were significantly increased(P<0.05)in the hypothalamus of rats with T2DM after DJB surgery.DJB surgery significantly reduced(P<0.05)hypothalamic inflammation in T2DM rats by inhibiting the activation of NF-κB and decreasing the expression of interleukin(IL)-1βand IL-6.DJB surgery significantly reduced(P<0.05)the expression of factors related to neuronal injury(glial fibrillary acidic protein and Caspase-3)in the hypothalamus of T2DM rats and upregulated(P<0.05)the expression of neuroprotective factors(C-fos,Ki67,Bcl-2,and BDNF),thereby reducing hypothalamic injury in T2DM rats.CONCLUSION DJB surgery improve oxidative stress and inflammation in the hypothalamus of T2DM rats and reduce neuronal cell injury by activating the glucagon-like peptide 1 receptor-mediated Nrf2/HO-1 signaling pathway. 展开更多
关键词 Duodenal jejunal bypass surgery Type 2 diabetes mellitus Neuron apoptosis INFLAMMATORY Oxidative stress Hypothalamic injury
下载PDF
A lead role for a“secondary”axonal injury response
13
作者 Melissa A.Rudy Trent A.Watkins 《Neural Regeneration Research》 SCIE CAS 2025年第2期469-470,共2页
Stress signaling following axon injury stimulates a transcriptional program for regeneration that might be exploited to promote central nervous system repair.However,this stress response drives neuronal apoptosis in n... Stress signaling following axon injury stimulates a transcriptional program for regeneration that might be exploited to promote central nervous system repair.However,this stress response drives neuronal apoptosis in non-regenerative environments.This duality presents a quandary for the development of therapeutic interventions:manipulating stress signaling to enhance recovery of damaged neurons risks accelerating neurodegeneration or restricting regenerative potential.This dichotomy is well illustrated by the fates of retinal ganglion cells(RGCs)following optic nerve crush.In this central nervous system injury model,disruption of a stress-activated MAP kinase(MAPK)cascade blocks the extensive apoptosis of RGCs that occurs in wild-type mice(Watkins et al.,2013;Welsbie et al.,2017). 展开更多
关键词 injury AXONAL stress
下载PDF
Acetaminophen overdose-induced acute liver injury can be alleviated by static magnetic field
14
作者 Han-Xiao Chen Xin-Yu Wang +11 位作者 Biao Yu Chuan-Lin Feng Guo-Feng Cheng Lei Zhang Jun-Jun Wang Ying Wang Ruo-Wen Guo Xin-Miao Ji Wen-Jing Xie Wei-Li Chen Chao Song Xin Zhang 《Zoological Research》 SCIE CSCD 2024年第3期478-490,共13页
Acetaminophen(APAP),the most frequently used mild analgesic and antipyretic drug worldwide,is implicated in causing 46%of all acute liver failures in the USA and between 40%and 70%in Europe.The predominant pharmacolog... Acetaminophen(APAP),the most frequently used mild analgesic and antipyretic drug worldwide,is implicated in causing 46%of all acute liver failures in the USA and between 40%and 70%in Europe.The predominant pharmacological intervention approved for mitigating such overdose is the antioxidant N-acetylcysteine(NAC);however,its efficacy is limited in cases of advanced liver injury or when administered at a late stage.In the current study,we discovered that treatment with a moderate intensity static magnetic field(SMF)notably reduced the mortality rate in mice subjected to high-dose APAP from 40%to 0%,proving effective at both the initial liver injury stage and the subsequent recovery stage.During the early phase of liver injury,SMF markedly reduced APAPinduced oxidative stress,free radicals,and liver damage,resulting in a reduction in multiple oxidative stress markers and an increase in the antioxidant glutathione(GSH).During the later stage of liver recovery,application of vertically downward SMF increased DNA synthesis and hepatocyte proliferation.Moreover,the combination of NAC and SMF significantly mitigated liver damage induced by high-dose APAP and increased liver recovery,even 24 h post overdose,when the effectiveness of NAC alone substantially declines.Overall,this study provides a noninvasive non-pharmaceutical tool that offers dual benefits in the injury and repair stages following APAP overdose.Of note,this tool can work as an alternative to or in combination with NAC to prevent or minimize liver damage induced by APAP,and potentially other toxic overdoses. 展开更多
关键词 ACETAMINOPHEN Acute liver injury Static magnetic fields Oxidative stress DNA synthesis
下载PDF
Placenta-derived mesenchymal stem cells attenuate secondary brain injury after controlled cortical impact in rats by inhibiting matrix metalloproteinases
15
作者 PING YANG YUANXIANG LAN +2 位作者 ZHONG ZENG YAN WANG HECHUN XIA 《BIOCELL》 SCIE 2024年第1期149-162,共14页
Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-t... Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-target and multi-pathway mode of action.Material&Methods:This study investigates the protective mechanisms and benefits of PDMSCs in mitigating the effects of controlled cortical impact(CCI)in rats and glutamate-induced oxidative stress injury in HT22 cells in vitro.Our primary objective is to provide evidence supporting the clinical application of PDMSCs.Results:In the in vivo arm of our investigation,we observed a swift elevation of matrix metalloproteinase-9(MMP-9)in the proximal cortex of injured brain tissues after CCI.PDMSCs,distinguished by their heightened expression of metalloproteinase tissue inhibitors-1 and-2(TIMP-1 and TIMP-2):were intravenously administered via the caudal vein.This intervention yielded significant reductions in the permeability of the blood-brain barrier(BBB):the extent of brain edema,the levels of inflammatory cytokines IL-1βand TNF-αin damaged brain tissue,and the activation status of microglia in CCI-afflicted rats.In the realm of in vitro experiments,PDMSC-conditioned media demonstrated substantial reductions in mortality rates and cleaved caspase-3 levels in glutamate-induced HT22 cells compared with conventional media.Notably,this advantage was negated upon the introduction of neutralizing antibodies targeting TIMP-1 and TIMP-2.Conclusion:Collectively,our findings underscore the potential of PDMSCs in alleviating oxidative stress injury and secondary brain injury in the pathological process of TBI. 展开更多
关键词 Traumatic brain injury Mesenchymal stem cells Oxidative stress Matrix metalloproteinases
下载PDF
Research Progress on the Pathogenesis of Acute Lung Injury(ALI)
16
作者 Jincun LI Wenyu MA Gang LI 《Medicinal Plant》 2024年第4期122-128,共7页
In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excess... In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excessive oxidative stress,cell death,endoplasmic reticulum stress,coagulation dysfunction,and weakened aquaporin function. 展开更多
关键词 Acute lung injury(ALI) Pathogenesis Inflammatory responses Oxidative stress Cell death Endoplasmic reticulum stress COAGULOPATHY Downregulation of aquaporin
下载PDF
Hypidone hydrochloride(YL-0919)ameliorates functional deficits after traumatic brain injury in mice by activating the sigma-1 receptor for antioxidation
17
作者 Yafan Bai Hui Ma +5 位作者 Yue Zhang Jinfeng Li Xiaojuan Hou Yixin Yang Guyan Wang Yunfeng Li 《Neural Regeneration Research》 SCIE CAS 2025年第8期2325-2336,共12页
Traumatic brain injury involves complex pathophysiological mechanisms,among which oxidative stress significantly contributes to the occurrence of secondary injury.In this study,we evaluated hypidone hydrochloride(YL-0... Traumatic brain injury involves complex pathophysiological mechanisms,among which oxidative stress significantly contributes to the occurrence of secondary injury.In this study,we evaluated hypidone hydrochloride(YL-0919),a self-developed antidepressant with selective sigma-1 receptor agonist properties,and its associated mechanisms and targets in traumatic brain injury.Behavioral experiments to assess functional deficits were followed by assessment of neuronal damage through histological analyses and examination of blood-brain barrier permeability and brain edema.Next,we investigated the antioxidative effects of YL-0919 by assessing the levels of traditional markers of oxidative stress in vivo in mice and in vitro in HT22 cells.Finally,the targeted action of YL-0919 was verified by employing a sigma-1 receptor antagonist(BD-1047).Our findings demonstrated that YL-0919 markedly improved deficits in motor function and spatial cognition on day 3 post traumatic brain injury,while also decreasing neuronal mortality and reversing blood-brain barrier disruption and brain edema.Furthermore,YL-0919 effectively combated oxidative stress both in vivo and in vitro.The protective effects of YL-0919 were partially inhibited by BD-1047.These results indicated that YL-0919 relieved impairments in motor and spatial cognition by restraining oxidative stress,a neuroprotective effect that was partially reversed by the sigma-1 receptor antagonist BD-1047.YL-0919 may have potential as a new treatment for traumatic brain injury. 展开更多
关键词 antidepressant drug blood-brain barrier cognitive function hypidone hydrochloride(YL-0919) neurological function nuclear factor-erythroid 2 related factor 2 oxidative stress sigma-1 receptor superoxide dismutase traumatic brain injury
下载PDF
Traumatic brain injury and variants of shock index
18
作者 Sai Doppalapudi Muhammad Adrish 《World Journal of Critical Care Medicine》 2024年第3期1-4,共4页
Traumatic Brain Injury is a major cause of death and long-term disability.The early identification of patients at high risk of mortality is important for both management and prognosis.Although many modified scoring sy... Traumatic Brain Injury is a major cause of death and long-term disability.The early identification of patients at high risk of mortality is important for both management and prognosis.Although many modified scoring systems have been developed for improving the prediction accuracy in patients with trauma,few studies have focused on prediction accuracy and application in patients with traumatic brain injury.The shock index(SI)which was first introduced in the 1960s has shown to strongly correlate degree of circulatory shock with increasing SI.In this editorial we comment on a publication by Carteri et al wherein they perform a retrospective analysis studying the predictive potential of SI and its variants in populations with severe traumatic brain injury. 展开更多
关键词 Predictive tools Traumatic brain injury Shock index Neurocardiogenic stress Myocardial ischemia
下载PDF
Chrysanthemum extract alleviates acetaminophen-induced liver injury by inhibiting oxidative stress via AMPK pathway in rats 被引量:1
19
作者 王春丽 谢欣梅 庞晓斌 《中国药理学与毒理学杂志》 CAS 北大核心 2019年第9期719-719,共1页
OBJECTIVE Acetaminophen(APAP),also known as paracetamol,is a commonly used antipyretic,anal⁃gesic and anti-inflammatory drug.However,during the use of APAP for more than half a century,people have not only used APAP t... OBJECTIVE Acetaminophen(APAP),also known as paracetamol,is a commonly used antipyretic,anal⁃gesic and anti-inflammatory drug.However,during the use of APAP for more than half a century,people have not only used APAP to fight diseases but have also suffered the adverse effects brought about by APAP for more than half a cen⁃tury.The most serious adverse reaction to APAP is hepatotoxicity caused by overdose or long-term use.In Chinese tra⁃ditional medicine,chrysanthemums have the functions of dispelling wind,dissipating heat,clearing the liver and improv⁃ing eyesight.Although the chrysanthemum variety named Bianliang ziyu from Kaifeng is not a medicinal variety,it has good value for medicine and food.The aim of this study was to investigate the protective effect of Bianliang Ziyu extract(BZE)on APAP-damaged rats and the potential molecular mechanism.METHODS Male Sprague-Dawley rats(200-220 g)were intragastrically administered BZE(110,220 and 440 mg·kg^-1)for 8 d.On the ninth day,APAP(800 mg·kg^-1)was administered intragastrically to the rats 0.5 h after BZE administration to induced drug-induced liver injury.The serum and liver samples were collected after 24 h.The levels of alanine aminotransferase(ALT),aspartic aminotransferase(AST),reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione(GSH)in serum and liver tissue of rats were detected by kit method.HE staining was used to observe the histopathological changes in the liver of rat.The effects of BZE on the expression of the oxidative stress related proteins and the mitochondrial biosyn⁃thesis related proteins were detected by Western blot.RESULTS The results showed that BZE significantly reduced the levels of ALT,AST,MDA and ROS and increased the levels of GSH and SOD caused by APAP.Moreover,BZE increased phosphorylation of AMP-activated protein kinase(AMPK)and glycogen synthase kinase 3β(GSK3β),promoted the nuclear translocation of nuclear factor-erythroid 2-related factor 2(Nrf2).BZE also upregulated the expression of mitochondrial biosynthesis related proteins such as peroxisome proliferator-activated receptorγ(PPAR-γ),peroxisome proliferator-activated receptorγcoactivator-1α(PGC-1α),mitochondrial transcription factor(TFAM)and nuclear respira⁃tory factor 1(NRF1).CONCLUSION BZE alleviates APAP-induced liver injury in rats by inhibiting oxidative stress via GSK3β-Nrf2 signaling and the mitochondrial biosynthesis pathway mediated by AMPK. 展开更多
关键词 ACETAMINOPHEN liver injury oxidative stress Chrysanthemum extract
下载PDF
Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities 被引量:58
20
作者 Jaime González-Montero Roberto Brito +1 位作者 Abraham IJ Gajardo Ramón Rodrigo 《World Journal of Cardiology》 CAS 2018年第9期74-86,共13页
Acute myocardial infarction(AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percut... Acute myocardial infarction(AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percutaneous coronary angioplasty(PCA) treatment, which quick-ly and effectively restore the blood flow to the area previously subjected to ischemia. Paradoxi-cally, the restoration of blood flow to the ischemic zone leads to a massive production of reactive oxygen species(ROS) which generate rapid and severe damage to biomolecules, generating a phenomenon called myocardial reperfusion injury(MRI). In the clinical setting, MRI is associated with multiple complications such as lethal reperfusion, no-reflow, myocardial stunning, and reperfusion arrhythmias. Despite significant advances in the understanding of the mechanisms accounting for the myocardial ischemia reperfusion injury, it remains an unsolved problem. Although promising results have been obtained in experimental studies(mainly in animal models), these benefits have not been translated into clinical settings. Thus, clinical trials have failed to find benefits from any therapy to prevent MRI. There is major evidence with respect to the contribution of oxidative stress to MRI in cardiovascular diseases. The lack- of consistency between basic studies and clinical trials is not solely based on the diversity inherent in epidemiology but is also a result of the methodological weak-nesses of some studies. It is quite possible that pharmacological issues, such as doses, active ingredients, bioavailability, routes of administration, co-therapies, startup time of the drug intervention,and its continuity may also have some responsibility for the lack- of consistency between different studies. Furthermore, the administration of high ascorbate doses prior to reperfusion appears to be a safe and rational therapy against the development of oxidative damage associated with myocardial reperfusion. In addition, the association with N-acetylcysteine(a glutathione donor) and deferoxamine(an iron chelator) could improve the antioxidant cardioprotection by ascorbate, mak-ing it even more effective in preventing myocardial reperfusion damage associated with PCA following AMI. 展开更多
关键词 Acute MYOCARDIAL INFARCTION Repefusion injury Oxidative stress ASCORBATE N-ACETYLCYSTEINE DEFEROXAMINE
下载PDF
上一页 1 2 234 下一页 到第
使用帮助 返回顶部