期刊文献+
共找到29,098篇文章
< 1 2 250 >
每页显示 20 50 100
Development of a new cerebral ischemia reperfusion model of Mongolian gerbils and standardized evaluation system 被引量:1
1
作者 Ying Wu Caijiao Hu +9 位作者 Zhihui Li Feiyang Li Jianyi Lv Meng Guo Xin Liu Changlong Li Xueyun Huo Zhenwen Chen Lifeng Yang Xiaoyan Du 《Animal Models and Experimental Medicine》 CAS CSCD 2024年第1期48-55,共8页
Background:The Mongolian gerbil is an excellent laboratory animal for preparing the cerebral ischemia model due to its inherent deficiency in the circle of Willis.However,the low incidence and unpredictability of symp... Background:The Mongolian gerbil is an excellent laboratory animal for preparing the cerebral ischemia model due to its inherent deficiency in the circle of Willis.However,the low incidence and unpredictability of symptoms are caused by numerous complex variant types of the circle.Additionally,the lack of an evaluation system for the cer-ebral ischemia/reperfusion(I/R)model of gerbils has shackled the application of this model.Methods:We created a symptom-oriented principle and detailed neurobehavioral scoring criteria.At different time points of reperfusion,we analyzed the alteration in locomotion by rotarod test and grip force score,infarct volume by triphenyltetrazo-lium chloride(TTC)staining,neuron loss using Nissl staining,and histological charac-teristics using hematoxylin-eosin(H&E)straining.Results:With a successful model rate of 56%,32 of the 57 gerbils operated by our method harbored typical features of cerebral I/R injury,and the mortality rate in the male gerbils was significantly higher than that in the female gerbils.The suc-cessfully prepared I/R gerbils demonstrated a significant reduction in motility and grip strength at 1 day after reperfusion;formed obvious infarction;exhibited typi-cal pathological features,such as tissue edema,neuronal atrophy and death,and vacuolated structures;and were partially recovered with the extension of reperfu-sion time.Conclusion:This study developed a new method for the unilateral common carotid artery ligation I/R model of gerbil and established a standardized evaluation system for this model,which could provide a new cerebral I/R model of gerbils with more practical applications. 展开更多
关键词 ISCHEMIA/reperfusion Mongolian gerbil standardized model system unilateral carotid occlusion
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:2
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
Homer1a reduces inflammatory response after retinal ischemia/reperfusion injury 被引量:1
3
作者 Yanan Dou Xiaowei Fei +7 位作者 Xin He Yu Huan Jialiang Wei Xiuquan Wu Weihao Lyu Zhou Fei Xia Li Fei Fei 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1608-1617,共10页
Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual damage.Homerla is repo rted to play a protective role in ... Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual damage.Homerla is repo rted to play a protective role in neuroinflammation in the cerebrum.However,the effects of Homerla on NLRP3inflammasomes in retinal ischemia/reperfusion injury caused by elevated IOP remain unknown.In our study,animal models we re constructed using C57BL/6J and Homer1^(flox/-)/Homerla^(+/-)/Nestin-Cre^(+/-)mice with elevated IOP-induced retinal ischemia/repe rfusion injury.For in vitro expe riments,the oxygen-glucose deprivation/repe rfusion injury model was constructed with M uller cells.We found that Homerla ove rexpression amelio rated the decreases in retinal thickness and Muller cell viability after ischemia/reperfusion injury.Furthermore,Homerla knockdown promoted NF-κB P65^(Ser536)activation via caspase-8,NF-κB P65 nuclear translocation,NLRP3 inflammasome formation,and the production and processing of interleukin-1βand inte rleukin-18.The opposite results we re observed with Homerla ove rexpression.Finally,the combined administration of Homerla protein and JSH-23 significantly inhibited the reduction in retinal thickness in Homer1^(flox/-)Homer1a^(+/-)/Nestin-Cre^(+/-)mice and apoptosis in M uller cells after ischemia/reperfusion injury.Taken together,these studies demonstrate that Homer1a exerts protective effects on retinal tissue and M uller cells via the caspase-8/NF-KB P65/NLRP3 pathway after I/R injury. 展开更多
关键词 CASPASE-8 Homer1a INTERLEUKIN-18 INTERLEUKIN-1Β intraocular pressure ischemia/reperfusion injury JSH-23 Müller cells NLRP3 nuclear factor-kB p65 RETINA
下载PDF
Cav3.2 channel regulates cerebral ischemia/reperfusion injury:a promising target for intervention 被引量:1
4
作者 Feibiao Dai Chengyun Hu +7 位作者 Xue Li Zhetao Zhang Hongtao Wang Wanjun Zhou Jiawu Wang Qingtian Geng Yongfei Dong Chaoliang Tang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第11期2480-2487,共8页
Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type ... Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type calcium channels.T-type calcium channel blockers,such as pimozide and mibefradil,have been shown to prevent cerebral ischemia/reperfusion injury-induced brain injury.However,the role of Cav3.2 channels in cerebral ischemia/reperfusion injury remains unclear.Here,in vitro and in vivo models of cerebral ischemia/reperfusion injury were established using middle cerebral artery occlusion in mice and high glucose hypoxia/reoxygenation exposure in primary hippocampal neurons.The results showed that Cav3.2 expression was significantly upregulated in injured hippocampal tissue and primary hippocampal neurons.We further established a Cav3.2 gene-knockout mouse model of cerebral ischemia/reperfusion injury.Cav3.2 knockout markedly reduced infarct volume and brain water content,and alleviated neurological dysfunction after cerebral ischemia/reperfusion injury.Additionally,Cav3.2 knockout attenuated cerebral ischemia/reperfusion injury-induced oxidative stress,inflammatory response,and neuronal apoptosis.In the hippocampus of Cav3.2-knockout mice,calcineurin overexpression offset the beneficial effect of Cav3.2 knockout after cerebral ischemia/reperfusion injury.These findings suggest that the neuroprotective function of Cav3.2 knockout is mediated by calcineurin/nuclear factor of activated T cells 3 signaling.Findings from this study suggest that Cav3.2 could be a promising target for treatment of cerebral ischemia/reperfusion injury. 展开更多
关键词 CALCINEURIN Cav3.2 channel cerebral ischemia/reperfusion hippocampus HYPOXIA/REOXYGENATION inflammatory response nuclear factor of activated T cells 3 oxidative stress primary hippocampal neurons stroke
下载PDF
Effects of high-dose glucose-insulin-potassium on acute coronary syndrome patients receiving reperfusion therapy:a meta-analysis
5
作者 Zeyu Yang Huiruo Liu +3 位作者 Dazhou Lu Shengchuan Cao Feng Xu Chuanbao Li 《World Journal of Emergency Medicine》 SCIE CAS CSCD 2024年第3期181-189,共9页
BACKGROUND:This meta-analysis aimed to assess the efficacy of high-dose glucose-insulinpotassium(GIK) therapy on clinical outcomes in acute coronary syndrome(ACS) patients receiving reperfusion therapy.METHODS:We sear... BACKGROUND:This meta-analysis aimed to assess the efficacy of high-dose glucose-insulinpotassium(GIK) therapy on clinical outcomes in acute coronary syndrome(ACS) patients receiving reperfusion therapy.METHODS:We searched the PubMed,Web of Science,MEDLINE,Embase,and Cochrane Library databases from inception to April 26,2022,for randomized controlled trials(RCTs) that compared high-dose GIK and placebos in ACS patients receiving reperfusion therapy.The primary endpoint was major adverse cardiovascular events(MACEs).RESULTS:Eleven RCTs with 884 patients were ultimately included.Compared with placebos,high-dose GIK markedly reduced MACEs(risk ratio [RR] 0.57,95% confidence interval [95% CI]:0.35 to 0.94,P=0.03) and the risk of heart failure(RR 0.48,95% CI:0.25 to 0.95,P=0.04) and improved the left ventricular ejection fraction(LVEF)(mean difference [MD] 2.12,95% CI:0.40 to 3.92,P=0.02) at 6 months.However,no difference was observed in all-cause mortality at 30 d or 1 year.Additionally,high-dose GIK was significantly associated with increased incidences of phlebitis(RR 4.78,95% CI:1.36 to 16.76,P=0.01),hyperglycemia(RR 9.06,95% CI:1.74 to 47.29,P=0.009) and hypoglycemia(RR 6.50,95% CI:1.28 to 33.01,P=0.02) but not reinfarction,hyperkalemia or secondary reperfusion.In terms of oxidative stress-lowering function,high-dose GIK markedly reduced superoxide dismutase(SOD) activity but not glutathione peroxidase(GSH-Px) or catalase(CAT) activity.CONCLUSION:Patients with ACS receiving reperfusion therapy exhibited a reduction in MACEs and good oxidative stress-lowering eflcacy in response to high-dose GIK.Moreover,with a higher incidence of complications such as phlebitis,hyperglycemia,and hypoglycemia.Furthermore,there were no observed survival benefits associated with high-dose GIK.More trials with long-term follow-up are still needed. 展开更多
关键词 Acute coronary syndrome HIGH-DOSE Glucose-insulin-potassium treatment reperfusion therapy META-ANALYSIS
下载PDF
Natural Products Improve Organ Microcirculation Dysfunction Following Ischemia/Reperfusion-and Lipopolysaccharide-Induced Disturbances:Mechanistic and Therapeutic Views
6
作者 Jingyan Han Quan Li +6 位作者 Kai Sun Chunshui Pan Jian Liu Ping Huang Juan Feng Yanchen Liu Gerald A.Meininger 《Engineering》 SCIE EI CAS CSCD 2024年第7期77-99,共23页
Microcirculatory disturbances are complex processes caused by many factors,including abnormal vasomotor responses,decreased blood flow velocity,vascular endothelial cell injury,altered leukocyte and endothelial cell i... Microcirculatory disturbances are complex processes caused by many factors,including abnormal vasomotor responses,decreased blood flow velocity,vascular endothelial cell injury,altered leukocyte and endothelial cell interactions,plasma albumin leakage,microvascular hemorrhage,and thrombosis.These disturbances involve multiple mechanisms and interactions among mechanisms that can include energy metabolism,the mitochondrial respiratory chain,oxidative stress,inflammatory factors,adhesion molecules,the cytoskeleton,vascular endothelial cells,caveolae,cell junctions,the vascular basement membrane,neutrophils,monocytes,and platelets.In clinical practice,aside from drugs that target abnormal vasomotor responses and platelet adhesion,there continues to be a lack of multi-target drugs that can regulate the complex mechanistic links and interactions underlying microcirculatory disturbances.Natural products have demonstrated obvious positive therapeutic effects in treating ischemia/reperfusion(I/R)-and lipopolysaccharide(LPS)-induced microcirculatory disturbances.In recent years,numerous research papers on the improvement of microcirculatory function by natural products have been published in international journals.In 2008 and 2017,the first listed author of this review was invited to publish reviews in the journal of Pharmacology&Therapeutics on the improvement of microcirculatory disturbances and organ injury induced by I/R using Salvia miltiorrhiza ingredients and other natural components of compounded Chinese medicine,respectively.This review systematically summarizes the effects,targets of action,and mechanisms of natural products regarding improving I/R-and LPSinduced microcirculatory disturbances and tissue injury.Based on this summary,scientific proposals are suggested for the discovery of new drugs to improve microcirculatory disturbances in disease. 展开更多
关键词 ISCHEMIA/reperfusion LIPOPOLYSACCHARIDE Natural products Leukocyte activation Hyperpermeability
下载PDF
Inhibition of SLC26A4 regulated by electroacupuncture suppresses the progression of myocardial ischemia-reperfusion injury
7
作者 FEI KONG QIYUAN TIAN +4 位作者 BINGLIN KUANG LILI SHANG XIAOXIAO ZHANG DONGYANG LI YING KONG 《BIOCELL》 SCIE 2024年第4期665-675,共11页
Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+in... Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+independent anion reverse transporter and has not been reported in myocardial IR injury.Objectives:Tofind potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury.Methods:RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment.Myocardial infarction size was detected by TTC staining.Serum CK,creatinine kinase-myocardial band,Cardiac troponin I,and lactate dehydrogenase levels were determined by ELISA.The effect of SLC26A4 on cardiomyocyte apoptosis was explored by TUNEL staining and western blotting.The effects of SLC26A4 on inflammation were determined by HE staining,ELISA,and real-time PCR.The effect of SLC26A4 on the NF-κB pathway was determined by western blotting.Results:SLC26A4 was up-regulated in IR rats but downregulated in IR rats with EA pretreatment.Compared with IR rats,those with SLC26A4 knockdown exhibited improved cardiac function according to decreased myocardial infarction size,reduced serum LDH/CK/CK-MB/cTnI levels,and elevated left ventricular ejection fraction and fractional shortening.SLC26A4 silencing inhibited myocardial inflammation,cell apoptosis,phosphorylation,and nuclear translocation of NF-κB p65.Conclusion:SLC26A4 exhibited promoting effects on myocardial IR injury,while the SLC26A4 knockdown had an inhibitory effect on the NF-κB pathway.These results further unveil the role of SLC26A4 in IR injury. 展开更多
关键词 Myocardial ischemia reperfusion SLC26A4 NF-κB pathway
下载PDF
Lactiplantibacillus plantarum AR113 alleviates microbiota dysbiosis of tongue coating and cerebral ischemia/reperfusion injury in rat
8
作者 Zhiqiang Xiong Gang Liu +5 位作者 Ling Fang Xiuming Li Yongjun Xia Guangqiang Wang Xin Song Lianzhong Ai 《Food Science and Human Wellness》 SCIE CAS CSCD 2024年第4期2132-2140,共9页
Stroke is one of the leading causes of death and disability worldwide.However,information on stroke-related tongue coating microbiome(TCM)is limited,and whether TCM modulation could benefit for stroke prevention and r... Stroke is one of the leading causes of death and disability worldwide.However,information on stroke-related tongue coating microbiome(TCM)is limited,and whether TCM modulation could benefit for stroke prevention and rehabilitation is unknown.Here,TCM from stroke patients(SP)was characterized using molecular techniques.The occurrence of stroke resulted in TCM dysbiosis with significantly reduced species richness and diversity.The abundance of Prevotella,Leptotrichia,Actinomyces,Alloprevotella,Haemophilus,and TM7_[G-1]were greatly reduced,but common infection Streptococcus and Pseudomonas were remarkably increased.Furthermore,an antioxidative probiotic Lactiplantibacillus plantarum AR113 was used for TCM intervention in stroke rats with cerebral ischemia/reperfusion(I/R).AR113 partly restored I/R induced change of TCM and gut microbiota with significantly improved neurological deficit,relieved histopathologic change,increased activities of antioxidant enzymes,and decreased contents of oxidative stress biomarkers.Moreover,the gene expression of antioxidant-related proteins and apoptosis-related factors heme oxygenase-1(HO-1),superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),nuclear factor erythroid 2-related factor 2(Nrf2),NAD(P)H:quinone oxidoreductase-1(NQO-1),and Bcl-2 was significantly increased,but cytochrome C,cleaved caspase-3,and Bax were markedly decreased in the brain by AR113 treatment.The results suggested that AR113 could ameliorate cerebral I/R injury through antioxidation and anti-apoptosis pathways,and AR113 intervention of TCM may have the application potential for stroke prevention and control. 展开更多
关键词 Stroke Cerebral ischemia/reperfusion Tongue coating Lactiplantibacillus plantarum AR113 Probiotic intervention
下载PDF
Long non-coding RNA-AK138945 regulates myocardial ischemia-reperfusion injury via the miR-1-GRP94 signaling pathway
9
作者 Yanying Wang Jian Huang +13 位作者 Han Sun Jie Liu Yingchun Shao Manyu Gong Xuewen Yang Dongping Liu Zhuo Wang Haodong Li Yanwei Zhang Xiyang Zhang Zhiyuan Du Xiaoping Leng Lei Jiao Ying Zhang 《Frigid Zone Medicine》 2024年第1期31-40,共10页
Objective:Myocardial ischemia-reperfusion injury(MIRI)is one of the leading causes of death from cardiovascular disease in humans,especially in individuals exposed to cold environments.Long non-coding RNAs(lncRNAs)reg... Objective:Myocardial ischemia-reperfusion injury(MIRI)is one of the leading causes of death from cardiovascular disease in humans,especially in individuals exposed to cold environments.Long non-coding RNAs(lncRNAs)regulate MIRI through multiple mechanisms.This study explored the regulatory effect of lncRNA-AK138945 on myocardial ischemia-reperfusion injury and its mechanism.Methods:In vivo,8-to 12-weeks-old C57BL/6 male mice underwent ligation of the left anterior descending coronary artery for 50 minutes followed by reperfusion for 48 hours.In vitro,the primary cultured neonatal mouse ventricular cardiomyocytes(NMVCs)were treated with 100μmol/L hydrogen peroxide(H_(2)O_(2)).The knockdown of lncRNA-AK138945 was evaluated to detect cardiomyocyte apoptosis,and a glucose-regulated,endoplasmic reticulum stress-related protein 94(GRP94)inhibitor was used to detect myocardial injury.Results:We found that the expression level of lncRNA-AK138945 was reduced in MIRI mouse heart tissue and H2O2-treated cardiomyocytes.Moreover,the proportion of apoptosis in cardiomyocytes increased after lncRNA-AK138945 was silenced.The expression level of Bcl2 protein was decreased,and the expression level of Bad,Caspase 9 and Caspase 3 protein was increased.Our further study found that miR-1a-3p is a direct target of lncRNA-AK138945,after lncRNA-AK138945 was silenced in cardiomyocytes,the expression level of miR-1a-3p was increased while the expression level of its downstream protein GRP94 was decreased.Interestingly,treatment with a GRP94 inhibitor(PU-WS13)intensified H2O2-induced cardiomyocyte apoptosis.After overexpression of FOXO3,the expression levels of lncRNA-AK138945 and GRP94 were increased,while the expression levels of miR-1a-3p were decreased.Conclusion:LncRNA-AK138945 inhibits GRP94 expression by regulating miR-1a-3p,leading to cardiomyocyte apoptosis.The transcription factor Forkhead Box Protein O3(FOXO3)participates in cardiomyocyte apoptosis induced by endoplasmic reticulum stress through up-regulation of lncRNA-AK138945. 展开更多
关键词 myocardial ischemia reperfusion lncRNA APOPTOSIS microRNAGRP94
下载PDF
Neuroprotective potential for mitigating ischemia-reperfusion-induced damage
10
作者 Zi Ye Runqing Liu +6 位作者 Hangxing Wang Aizhen Zuo Cen Jin Nan Wang Huiqi Sun Luqian Feng Hua Yang 《Neural Regeneration Research》 SCIE CAS 2025年第8期2199-2217,共19页
Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion injury.Curre... Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion injury.Current studies have elucidated the neuroprotective role of the sirtuin protein family(Sirtuins)in modulating cerebral ischemia-reperfusion injury.However,the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration.In this review,the origin and research progress of Sirtuins are summarized,suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury,including inflammation,oxidative stress,blood-brain barrier damage,apoptosis,pyroptosis,and autophagy.The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways,such as nuclear factor-kappa B signaling,oxidative stress mediated by adenosine monophosphate-activated protein kinase,and the forkhead box O.This review also summarizes the potential of endogenous substances,such as RNA and hormones,drugs,dietary supplements,and emerging therapies that regulate Sirtuins expression.This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors.While Sirtuins show promise as a potential target for the treatment of cerebral ischemiareperfusion injury,most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans,potentially influencing the efficacy of Sirtuinstargeting drug therapies.Overall,this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury. 展开更多
关键词 apoptosis autophagy blood-brain barrier dietary supplements drug HORMONES inflammation NEUROPROTECTION oxidative stress prognosis PYROPTOSIS reperfusion injury risk factors RNA THERAPEUTICS
下载PDF
Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention
11
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
The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice
12
作者 Bo Zhao Mei Li +6 位作者 Bingyu Li Yanan Li Qianni Shen Jiabao Hou Yang Wu Lijuan Gu Wenwei Gao 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2019-2026,共8页
Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of... Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway. 展开更多
关键词 brain C1q/tumor necrosis factor-related protein-6 cerebral apoptosis diabetes inflammation ischemia/reperfusion injury NEURON NEUROPROTECTION oxidative damage Sirt1
下载PDF
A matrix metalloproteinase-responsive hydrogel system controls angiogenic peptide release for repair of cerebral ischemia/reperfusion injury
13
作者 Qi Liu Jianye Xie +5 位作者 Runxue Zhou Jin Deng Weihong Nie Shuwei Sun Haiping Wang Chunying Shi 《Neural Regeneration Research》 SCIE CAS 2025年第2期503-517,共15页
Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug deliv... Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug delivery often results in a burst release of the drug,leading to transient retention(inefficacy)and undesirable diffusion(toxicity)in vivo.Therefore,a drug delivery system that responds to changes in the microenvironment of tissue regeneration and controls vascular endothelial growth factor release is crucial to improve the treatment of ischemic stroke.Matrix metalloproteinase-2(MMP-2)is gradually upregulated after cerebral ischemia.Herein,vascular endothelial growth factor mimic peptide QK was self-assembled with MMP-2-cleaved peptide PLGLAG(TIMP)and customizable peptide amphiphilic(PA)molecules to construct nanofiber hydrogel PA-TIMP-QK.PA-TIMP-QK was found to control the delivery of QK by MMP-2 upregulation after cerebral ischemia/reperfusion and had a similar biological activity with vascular endothelial growth factor in vitro.The results indicated that PA-TIMP-QK promoted neuronal survival,restored local blood circulation,reduced blood-brain barrier permeability,and restored motor function.These findings suggest that the self-assembling nanofiber hydrogel PA-TIMP-QK may provide an intelligent drug delivery system that responds to the microenvironment and promotes regeneration and repair after cerebral ischemia/reperfusion injury. 展开更多
关键词 angiogenesis biomaterial blood-brain barrier cerebral ischemia/reperfusion injury control release drug delivery inflammation QK peptides matrix metalloproteinase-2 NEUROPROTECTION self-assembling nanofiber hydrogel
下载PDF
N-acetylserotonin alleviates retinal ischemia-reperfusion injury via HMGB1/RAGE/NF-κB pathway in rats
14
作者 Yu-Ze Zhao Xue-Ning Zhang +7 位作者 Yi Yin Pei-Lun Xiao Meng Gao Lu-Ming Zhang Shuan-Hu Zhou Shu-Na Yu Xiao-Li Wang Yan-Song Zhao 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2024年第2期228-238,共11页
AIM:To observe the effects of N-acetylserotonin(NAS)administration on retinal ischemia-reperfusion(RIR)injury in rats and explore the underlying mechanisms involving the high mobility group box 1(HMGB1)/receptor for a... AIM:To observe the effects of N-acetylserotonin(NAS)administration on retinal ischemia-reperfusion(RIR)injury in rats and explore the underlying mechanisms involving the high mobility group box 1(HMGB1)/receptor for advanced glycation end-products(RAGE)/nuclear factor-kappa B(NF-κB)signaling pathway.METHODS:A rat model of RIR was developed by increasing the pressure of the anterior chamber of the eye.Eighty male Sprague Dawley were randomly divided into five groups:sham group(n=8),RIR group(n=28),RIR+NAS group(n=28),RIR+FPS-ZM1 group(n=8)and RIR+NAS+FPS-ZM1 group(n=8).The therapeutic effects of NAS were examined by hematoxylin-eosin(H&E)staining,and retinal ganglion cells(RGCs)counting.The expression of interleukin 1 beta(IL-1β),HMGB1,RAGE,and nod-like receptor 3(NLRP3)proteins and the phosphorylation of nuclear factorkappa B(p-NF-κB)were analyzed by immunohistochemistry staining and Western blot analysis.The expression of HMGB1 protein was also detected by enzyme-linked immunosorbent assay(ELISA).RESULTS:H&E staining results showed that NAS significantly reduced retinal edema and increased the number of RGCs in RIR rats.With NAS therapy,the HMGB1 and RAGE expression decreased significantly,and the activation of the NF-κB/NLRP3 pathway was antagonized along with the inhibition of p-NF-κB and NLRP3 protein expression.Additionally,NAS exhibited an anti-inflammatory effect by reducing IL-1βexpression.The inhibitory of RAGE binding to HMGB1 by RAGE inhibitor FPS-ZM1 led to a significant decrease of p-NF-κB and NLRP3 expression,so as to the IL-1βexpression and retinal edema,accompanied by an increase of RGCs in RIR rats.CONCLUSION:NAS may exhibit a neuroprotective effect against RIR via the HMGB1/RAGE/NF-κB signaling pathway,which may be a useful therapeutic target for retinal disease. 展开更多
关键词 retinal diseases retinal ischemia—reperfusion injury N-ACETYLSEROTONIN high mobility group box 1 receptor for advanced glycation end-products nuclear factor-κB RATS
下载PDF
瑞马唑仑调节HIF-1α/BNIP3信号通路对OGD/R诱导神经细胞自噬和凋亡的影响
15
作者 王效德 后晓超 +3 位作者 李青青 司玉婷 周小平 徐桂萍 《河北医药》 CAS 2024年第8期1138-1141,1146,共5页
目的探讨瑞马唑仑对OGD/R诱导的神经细胞自噬和凋亡的影响及作用机制。方法体外培养小鼠海马神经元细胞(HT22)并进行神经细胞氧糖剥夺/再复氧(OGD/R),筛选实验用瑞马唑仑浓度;将HT22细胞分为对照组、OGD/R组、瑞马唑仑组、2-ME2组、瑞... 目的探讨瑞马唑仑对OGD/R诱导的神经细胞自噬和凋亡的影响及作用机制。方法体外培养小鼠海马神经元细胞(HT22)并进行神经细胞氧糖剥夺/再复氧(OGD/R),筛选实验用瑞马唑仑浓度;将HT22细胞分为对照组、OGD/R组、瑞马唑仑组、2-ME2组、瑞马唑仑+2-ME2组;CCK8法检测5组HT22细胞活力;流式细胞术检测5组HT22细胞凋亡率;透射电子显微镜观察5组HT22细胞自噬小体的形成;Western blot检测5组HT22细胞HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ的表达。结果确定实验用瑞马唑仑浓度为50μg/mL;与对照组比较,OGD/R组HT22细胞OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平下调,凋亡率上调(P<0.05);与OGD/R组比较,瑞马唑仑组HT22细胞自噬小体增加,OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平上调,凋亡率下调(P<0.05);2-ME2组HT22细胞OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平下调,凋亡率上调(P<0.05)。与瑞马唑仑组比较,瑞马唑仑+2-ME2组HT22细胞自噬小体数量减少,OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平下调,凋亡率上调(P<0.05);与2-ME2组比较,瑞马唑仑+2-ME2组HT22细胞OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平上调,凋亡率下调(P<0.05)。结论瑞马唑仑可通过激活HIF-1α/BNIP3信号通路促进OGD/R诱导的神经细胞自噬,抑制细胞凋亡,从而减轻OGD/R诱导的神经细胞损伤。 展开更多
关键词 瑞马唑仑 HIF-1α/BNIP3信号通路 ogd/R诱导的神经细胞 自噬 凋亡
下载PDF
右美托咪定通过抑制RIPK/MLKL通路减轻OGD/R诱导的神经元坏死性凋亡
16
作者 孙凯 《河南外科学杂志》 2024年第1期41-44,共4页
目的评价右美托咪定对氧糖剥夺/再灌注(OGD/R)诱导的HT22神经元细胞坏死性凋亡的影响。方法体外培养HT22小鼠海马神经元细胞,建立OGD/R模型。细胞分为对照组,OGD/R模型组,右美托咪定低、中、高浓度组(2.5、5、10μM)。采用CCK-8测定细... 目的评价右美托咪定对氧糖剥夺/再灌注(OGD/R)诱导的HT22神经元细胞坏死性凋亡的影响。方法体外培养HT22小鼠海马神经元细胞,建立OGD/R模型。细胞分为对照组,OGD/R模型组,右美托咪定低、中、高浓度组(2.5、5、10μM)。采用CCK-8测定细胞存活率,乳酸脱氢酶(LDH)试剂盒检测细胞上清LDH含量,流式细胞仪检测细胞凋亡,RT-qPCR和免疫印迹检测坏死性凋亡关键因子受体相互作用蛋白激酶1(RIPK1)和混合系列蛋白激酶样结构域(MLKL)的mRNA和蛋白表达水平。结果与对照组比较,OGD/R模型组细胞存活率显著降低(P<0.001),上清LDH含量和细胞凋亡率、RIPK1和MLKL的mRNA和蛋白表达水平均显著升高(P<0.01);与OGD/R模型组比较,右美托咪定5和10μM显著提高了细胞存活率,减少了LDH含量和凋亡率,下调RIPK1和MLKL的mRNA和蛋白表达水平(P均<0.01)。结论右美托咪定可减轻OGD/R诱导的神经元损伤,其机制可能与抑制RIPK1/MLKL通路介导的坏死性凋亡有关。 展开更多
关键词 右美托咪定 ogd/R HT22细胞 坏死性凋亡
下载PDF
小续命汤对OGD/R诱导HT22细胞损伤后突触可塑性的影响 被引量:3
17
作者 王漫漫 兰瑞 +6 位作者 张勇 付雪琴 邹旭欢 王玮玮 李泓宇 唐琛 刘双 《中国病理生理杂志》 CAS CSCD 北大核心 2024年第1期126-133,共8页
目的:探讨小续命汤(XXMD)对缺血性脑卒中后脑缺血再灌注损伤突触可塑性的影响。方法:体外建立小鼠海马神经元(HT22细胞)氧糖剥夺/复氧(OGD/R)模型,模拟脑缺血性脑卒中后海马神经元缺血再灌注损伤。采用CCK-8法检测HT22细胞活力,筛选XXM... 目的:探讨小续命汤(XXMD)对缺血性脑卒中后脑缺血再灌注损伤突触可塑性的影响。方法:体外建立小鼠海马神经元(HT22细胞)氧糖剥夺/复氧(OGD/R)模型,模拟脑缺血性脑卒中后海马神经元缺血再灌注损伤。采用CCK-8法检测HT22细胞活力,筛选XXMD最佳作用浓度。将HT22细胞随机分为对照组、OGD/R组和OGD/R+XXMD组,倒置荧光显微镜观察各组细胞形态变化,ELISA法测定细胞上清液中炎症因子IL-1β、IL-6和TNF-α水平,透射电镜观察细胞超微结构改变,免疫荧光染色检测神经元标志物Neu N及突触相关蛋白NF200和MAP2的荧光强度,Western blot检测各组细胞中NF200和MAP2蛋白表达水平。结果:XXMD在浓度为100 mg/L时细胞活力最强(P<0.05)。与对照组相比,模型组细胞变圆皱缩,线粒体呈现肿胀甚至空泡样改变,活力明显下降(P<0.05),IL-1β、IL-6和TNF-α含量升高(P<0.05),NF200和MAP2的荧光强度及蛋白表达水平显著降低(P<0.05)。而XXMD可改善细胞形态及超微结构,提升生存率(P<0.05),降低炎症因子水平(P<0.05)。免疫荧光染色及Western blot结果显示,与模型组相比,OGD/R+XXMD组可以增强NF200和MAP2平均荧光强度(P<0.05),提升蛋白表达水平(P<0.05)。结论:XXMD可以减轻OGD/R诱导的HT22细胞损伤,其机制可能涉及减轻炎症反应和增强突触可塑性。 展开更多
关键词 小续命汤 氧糖剥夺 HT22细胞 缺血性脑卒中 突触可塑性
下载PDF
Reperfusion after hypoxia-ischemia exacerbates brain injury with compensatory activation of the antiferroptosis system:based on a novel rat model 被引量:3
18
作者 Tian-Lei Zhang Zhi-Wei Zhang +6 位作者 Wei Lin Xin-Ru Lin Ke-Xin Lin Ming-Chu Fang Jiang-Hu Zhu Xiao-Ling Guo Zhen-Lang Lin 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第10期2229-2236,共8页
Hypoxic-ischemic encephalopathy,which predisposes to neonatal death and neurological sequelae,has a high morbidity,but there is still a lack of effective prevention and treatment in clinical practice.To better underst... Hypoxic-ischemic encephalopathy,which predisposes to neonatal death and neurological sequelae,has a high morbidity,but there is still a lack of effective prevention and treatment in clinical practice.To better understand the pathophysiological mechanism underlying hypoxic-ischemic encephalopathy,in this study we compared hypoxic-ischemic reperfusion brain injury and simple hypoxic-ischemic brain injury in neonatal rats.First,based on the conventional RiceVannucci model of hypoxic-ischemic encephalopathy,we established a rat model of hypoxic-ischemic reperfusion brain injury by creating a common carotid artery muscle bridge.Then we performed tandem mass tag-based proteomic analysis to identify differentially expressed proteins between the hypoxic-ischemic reperfusion brain injury model and the conventional Rice-Vannucci model and found that the majority were mitochondrial proteins.We also performed transmission electron microscopy and found typical characteristics of ferroptosis,including mitochondrial shrinkage,ruptured mitochondrial membranes,and reduced or absent mitochondrial cristae.Further,both rat models showed high levels of glial fibrillary acidic protein and low levels of myelin basic protein,which are biological indicators of hypoxic-ischemic brain injury and indicate similar degrees of damage.Finally,we found that ferroptosis-related Ferritin(Fth1)and glutathione peroxidase 4 were expressed at higher levels in the brain tissue of rats with hypoxic-ischemic reperfusion brain injury than in rats with simple hypoxic-ischemic brain injury.Based on these results,it appears that the rat model of hypoxic-ischemic reperfusion brain injury is more closely related to the pathophysiology of clinical reperfusion.Reperfusion not only aggravates hypoxic-ischemic brain injury but also activates the anti-ferroptosis system. 展开更多
关键词 ferroptosis hypoxic-ischemic brain injury hypoxic-ischemic encephalopathy hypoxic-ischemic reperfusion brain injury mitochondria model proteomic analysis reperfusion Rice-Vannucci transmission electron microscopy
下载PDF
Ischemic accumulation of succinate induces Cdc42 succinylation and inhibits neural stem cell proliferation after cerebral ischemia/reperfusion 被引量:3
19
作者 Lin-Yan Huang Ju-Yun Ma +9 位作者 Jin-Xiu Song Jing-Jing Xu Rui Hong Hai-Di Fan Heng Cai Wan Wang Yan-Ling Wang Zhao-Li Hu Jian-Gang Shen Su-Hua Qi 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第5期1040-1045,共6页
Ischemic accumulation of succinate causes cerebral damage by excess production of reactive oxygen species. However, it is unknown whether ischemic accumulation of succinate affects neural stem cell proliferation. In t... Ischemic accumulation of succinate causes cerebral damage by excess production of reactive oxygen species. However, it is unknown whether ischemic accumulation of succinate affects neural stem cell proliferation. In this study, we established a rat model of cerebral ischemia/reperfusion injury by occlusion of the middle cerebral artery. We found that succinate levels increased in serum and brain tissue(cortex and hippocampus) after ischemia/reperfusion injury. Oxygen-glucose deprivation and reoxygenation stimulated primary neural stem cells to produce abundant succinate. Succinate can be converted into diethyl succinate in cells. Exogenous diethyl succinate inhibited the proliferation of mouse-derived C17.2 neural stem cells and increased the infarct volume in the rat model of cerebral ischemia/reperfusion injury. Exogenous diethyl succinate also increased the succinylation of the Rho family GTPase Cdc42 but repressed Cdc42 GTPase activity in C17.2 cells. Increasing Cdc42 succinylation by knockdown of the desuccinylase Sirt5 also inhibited Cdc42 GTPase activity in C17.2 cells. Our findings suggest that ischemic accumulation of succinate decreases Cdc42 GTPase activity by induction of Cdc42 succinylation, which inhibits the proliferation of neural stem cells and aggravates cerebral ischemia/reperfusion injury. 展开更多
关键词 CDC42 cerebral ischemia/reperfusion injury GPR91 neural stem cells neurogenesis PROLIFERATION SIRT5 SUCCINATE SUCCINYLATION
下载PDF
Do reactive oxygen species damage or protect the heart in ischemia and reperfusion?Analysis on experimental and clinical data 被引量:1
20
作者 Leonid N.Maslov Natalia V.Naryzhnaya +9 位作者 Maria Sirotina Alexandr V.Mukhomedzyanov Boris K.Kurbatov Alla A.Boshchenko Huijie Ma Yi Zhang Feng Fu Jianming Pei Viacheslav N.Azev Vladimir A.Pereverzev 《The Journal of Biomedical Research》 CAS CSCD 2023年第4期255-267,共13页
The role of reactive oxygen species(ROS)in ischemic and reperfusion(I/R)injury of the heart has been discussed for more than 40 years.It has been demonstrated that reperfusion triggers a multiple increase in free radi... The role of reactive oxygen species(ROS)in ischemic and reperfusion(I/R)injury of the heart has been discussed for more than 40 years.It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart.Antioxidants were found to have the ability to mitigate I/R injury of the heart.However,it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues.Since high doses and high concentrations of antioxidants were experimentally used,it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules.It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning.Consequently,there is evidence that ROS protect the heart against the I/R injury. 展开更多
关键词 reactive oxygen species free radicals ANTIOXIDANTS HEART reperfusion patients
下载PDF
上一页 1 2 250 下一页 到第
使用帮助 返回顶部