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Ischemic Postconditioning Alleviates Cerebral Ischemia-Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats 期刊论文

编号：

74f57760-1b59-4a5f-b3bc-22375197989f
作者：

Sun, Yameng(孙亚蒙)#^[1]Zhang, Ting(张婷)^[1]Zhang, Yan^[2]Li, Jinfeng(李晋峰)^[2]Jin, Lei(金磊)^[2]Sun, Yinyi(孙寅轶)^[1]Shi, Nan(史楠)^[2]Liu, Kangyong(刘康永)*^[2]Sun, Xiaojiang(孙晓江)*^[1]
语种：

英文
期刊：

NEUROCHEMICAL RESEARCH ISSN：0364-3190 2018 年 43 卷 9 期 (1826 - 1840) ; SEP
收录：
关键词：

Ischemic postconditioning Autophagy flux Cerebral ischemia-reperfusion injury Mitochondrial dysfunction
摘要：

This study aimed to investigate whether ischemic postconditioning (IpostC) alleviates cerebral ischemia/reperfusion (I/R) injury involved in autophagy. Adult Sprague-Dawley rats were divided into five groups: sham (sham surgery), I/R (middle cerebral artery occlusion [MCAO] for 100 min, then reperfusion), IpostC (MCAO for 100 min, reperfusion for 10 min, MCAO for 10 min, then reperfusion), IpostC+3MA (3-methyladenine, an autophagy inhibitor, administered 30 min before first reperfusion), and IpostC+Veh (vehicle control for IpostC+3MA group). Infarct volume was measured using cresyl violet staining. Autophagy-related proteins were detected by western blot and immunohistochemistry. Autophagosomes, autophagolysosomes, and mitochondrial damage were identified by transmission electron microscopy. Cortical cell apoptosis was detected by the TUNEL assay. Neurologic function was assessed using the modified Neurologic Severity Score. IpostC improved neurological function and reduced infarct volume after I/R (P < 0.05). These effects of IpostC were inhibited by 3MA (P < 0.05). Autophagosome formation was increased in the I/R and IpostC+Veh groups (P < 0.05), but not in the IpostC+3MA group. The I/R group showed enhanced LC3-II/LC3-I ratio, p62, and Cathepsin B levels and decreased LAMP-2 level (all P < 0.05 vs. sham), indicating dysfunction of autophagic clearance. IpostC reduced p62 and Cathepsin B levels and increased the LC3-II/LC3-I ratio, and nuclear translocation of transcription factor EB (all P < 0.05); these effects of IpostC were reversed by 3MA, suggesting IpostC enhanced autophagic flux. Furthermore, IpostC attenuated I/R-induced mitochondrial translocation of Bax and mitochondrial cytochrome-c release (all P < 0.05); 3MA inhibited these effects of IpostC (P < 0.05). In conclusion, IpostC may alleviate cerebral I/R injury by activating autophagy during early reperfusion.
推荐引用方式
GB/T 7714：

Sun Yameng,Zhang Ting,Zhang Yan, et al. Ischemic Postconditioning Alleviates Cerebral Ischemia-Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats [J].NEUROCHEMICAL RESEARCH,2018,43(9):1826-1840.
APA：

Sun Yameng,Zhang Ting,Zhang Yan,Li Jinfeng,&Sun Xiaojiang.(2018).Ischemic Postconditioning Alleviates Cerebral Ischemia-Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats .NEUROCHEMICAL RESEARCH,43(9):1826-1840.
MLA：

Sun Yameng, et al. "Ischemic Postconditioning Alleviates Cerebral Ischemia-Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats" .NEUROCHEMICAL RESEARCH 43,9(2018):1826-1840.
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