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白藜芦醇通过激活PI3K/Akt信号通路减轻大鼠脑缺血再灌注损伤
引用本文:雷军荣,涂献坤,张华斌,张,晶,秦,军,罗,杰,石松生,杨卫忠.白藜芦醇通过激活PI3K/Akt信号通路减轻大鼠脑缺血再灌注损伤[J].中国临床神经外科杂志,2016,0(7):425-428.
作者姓名:雷军荣  涂献坤  张华斌              石松生  杨卫忠
作者单位:442000 十堰,湖北医药学院附属十堰市太和医院神经外科(雷军荣、张 晶、秦 军、罗 杰);350001 福州,福建医科大学附属协和医院神经外科(涂献坤、张华斌、松生、杨卫忠) 通讯作者:涂献坤,E-mail:tuxiankun@163.com
摘    要:目的 探讨PI3K/Akt信号通路在白藜芦醇减轻大鼠脑缺血再灌注损伤中的作用。方法 将48只成年SD大鼠随机分为假手术组、模型组、白藜芦醇组、LY294002组(Akt抑制剂),每组12只。利用线栓法制备大鼠脑缺血再灌注损伤模型,造模后24 h进行大鼠神经功能损伤评分和检测脑梗死体积、脑组织髓过氧化物酶(MPO)的活性,免疫印迹法检测脑组织p-Akt、t-Akt的表达水平,ELISA法检测脑组织肿瘤坏死因子-α(TNF-α)的含量。结果 与假手术组相比,模型组大鼠神经功能损伤评分、脑梗死体积、缺血脑组织MPO活性和TNF-α含量均明显增高(P<0.05),缺血脑组织p-Akt表达水平也明显增高(P<0.05);与模型组相比,白藜芦醇显著降低大鼠神经功能损伤评分、脑梗死体积、缺血脑组织MPO活性和TNF-α含量(P<0.05),也显著降低缺血脑组织p-Akt表达水平(P<0.05);脑室内注射LY294002,显著抑制白藜芦醇的这些作用(P<0.05)。结论 白藜芦醇通过激活PI3K/Akt信号通路减轻大鼠脑缺血再灌注损伤。

关 键 词:脑缺血再灌注  白藜芦醇  炎症反应  PI3K/Akt  大鼠

Resveratrol reduces cerebral ischemia-reperfusion injury through the activation of PI3K/Akt signaling pathway in rats
LEI Jun-rong,TU Xian-kun,ZHANG Hua-bin,ZHANG Jing,QIN Jun,LUO Jie,SHI Song-sheng,YANG Wei-zhong..Resveratrol reduces cerebral ischemia-reperfusion injury through the activation of PI3K/Akt signaling pathway in rats[J].Chinese Journal of Clinical Neurosurgery,2016,0(7):425-428.
Authors:LEI Jun-rong  TU Xian-kun  ZHANG Hua-bin  ZHANG Jing  QIN Jun  LUO Jie  SHI Song-sheng  YANG Wei-zhong
Institution:1. Department of Neurosurgery, Affiliated Hospital, Hubei University of Medicine, Shiyan 442000, China; 2. Department of Neurosurgery, Union Hospital, Fujian Medical University, Fuzhou 350001, China
Abstract:Objective To study the effect of resveratrol on cerebral injury induced by ischemic-reperfusion and its mechanism in rats. Methods Forty-eight SD rats were randomly divided into 4 groups of 12 animals each, including sham operation group, control group, experimental groupⅠin which the animal received the intraperitoneal injection of resveratrol 2 hours after the cerebral ischemia, and experimental group Ⅱ in which the animal received the intraventricular injection of LY294002 before the cerebral ischemia and the intraperitoneal injection of resveratrol 2 hours after the cerebral ischemia- reperfusion. The ischemia-reperfusion models were made by the suture occlusion in the control group, and experimental groups Ⅰ and Ⅱ. Neurological deficit scores, cerebral infarct volume and myeloperoxidase (MPO) activity in injured cerebral tissues were assessed 24 hours after cerebral ischemia-reperfusion. The expressions of p-Akt and t-Akt and content of tumor necrosis factor-α (TNF-α) in the injured cerebral tissues were detected by western blot and ELISA respectively in all the groups. Results The neurological deficit scores and cerebral infarct volume were significantly bigger in the control group 24 hours after the ischemia-reperfusion than those in the experimental group Ⅰ(P<0.05), which were significantly smaller in the experimental group Ⅱ. The level of MPO activity and TNF-α in the injured cerebral tissues were significantly higher in the control group than those in the experimental groupⅡ(P<0.05), which were significantly higher in experimental groupⅠ(P<0.05), which were significantly higher in sham operation group (P<0.05). The levels of p-Akt and t-Akt expressions in the injured cerebral tissues were significantly higher in experimental group Ⅰthan those in experimental group Ⅱ(P<0.05), which were significantly higher in control group (P<0.05). Conclusions It is suggested that resveratrol can reduce cerebral ischemic-reperfusion injury and inflammatory reaction through the activation of PI3K/Akt signaling pathway in the rats.
Keywords:Cerebral ischemia-reperfusion  Resveratrol  Inflammatory reaction  PI3K/Akt  Rats
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