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探讨针刺水沟和内关对局灶性脑缺血再灌注大鼠PI3K/Akt信号通路的影响
引用本文:张丽丽,刘宝山,杜宇征,褚芹. 探讨针刺水沟和内关对局灶性脑缺血再灌注大鼠PI3K/Akt信号通路的影响[J]. 辽宁中医杂志, 2012, 0(11): 2308-2311
作者姓名:张丽丽  刘宝山  杜宇征  褚芹
作者单位:天津中医药大学;天津中医药大学第一附属医院
基金项目:国家自然科学基金资助项目(30873301)
摘    要:目的:了解局灶性脑缺血再灌注后大鼠脑内PI3K、p-Akt及Caspase3的动态变化,以及针刺水沟、内关对其表达的影响。方法:采用改良的线栓法制备大脑中动脉阻塞1h,不同再灌注时间段(6h、1天、3天、5天、7天)的大鼠短暂局灶性脑缺血模型。应用TUNEL测定不同时点神经细胞凋亡情况,免疫组化和western blot测定不同时点蛋白的表达情况。结果:脑缺血再灌注后1天凋亡细胞百分率、PI3K、p-Akt水平达到峰值,而针刺水沟、内关组凋亡细胞百分率略低于同时点的对照组,相应蛋白表达水平较相同时点对照组增强;在灌注后3天Caspase3达到高峰,而针刺水沟和内关组其表达水平较对照组降低。结论:针刺水沟、内关的神经保护作用可能与PI3K/Akt信号通路有关。

关 键 词:针刺  缺血再灌注  PI3K  p-Akt  Caspase3

Effect of Needling Shuigou and Neiguan on PI3K/Akt Signaling Pathway in Focal Cerebral Ischemia/Reperfusion Rats
Affiliation:ZHANG Li-li1,LIU Bao-shan2,DU Yu-zheng2,HU Qin2(1.Tianjin University of Traditional Chinese Medicine,Tianjin 300193,China; 2.The First Affiliated Hospital of Tianjin University of Traditional Chinese Medicine,Tianjin 300193,China)
Abstract:Objective:To explore the changes of PI3K,p-Akt and Caspase3 and the effect of needling Shuigou(DU26)and Neiguan(PC6)on it after the focal ischemia/ reperfusion.Methods:The model of ischemia/reperfusion in rats was made by middle cerebral artery occlusion.Adult Sprague-Dawley rats received occlusion of the left middle cerebral artery for 60min then reperfusion was made for 6h,1d,3d,5d,7d respectively.The apoptotic cells were assessed by TUNEL method.The expressions of PI3K,p-Akt and Caspase3 were evaluated by western blotting at different time points.Results:The percentage of apoptotic cells,the expressions of PI3K and p-Akt reached the peak one day after the reperfusion,while that of Caspase3 reached the peak three days after the reperfusion.Needling Shuigou(DU26)and Neiguan(PC6)made the expressions of PI3K and p-Akt higher,but expression of Caspase3 lower than that in the control groups at different time points.Conclusion:The neuroprotective effect of needling Shuigou(DU26)and Neiguan(PC6)may be related to the PI3K/Akt signaling pathway.
Keywords:needling  ischemia/ reperfusion  PI3K  p-Akt  Caspase3
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