• 论文检测软件 > 优秀论文akt 信号通路与二氮嗪预处理抗缺氧复氧后大鼠海马神经元凋
  • 优秀论文akt 信号通路与二氮嗪预处理抗缺氧复氧后大鼠海马神经元凋

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    2008 年中华医学会全国麻醉学术年会
    优秀论文 Akt 信号通路与二氮嗪预处理抗缺氧复氧后大鼠海马神经元 凋亡作用关系的研究
    福建省立医院麻醉科(福建福州,350001) 李捷萌 陈彦青 刘荣国 吴晓丹
    目的: 探讨 Akt 信号通路与二氮嗪预处理抗缺氧复氧后大鼠海马神经元凋亡作用的关系. 方法: 取离体培养的大鼠海马神经元,随机分为 6 组:对照组(A 组) ,缺氧组(B 组) ,缺氧+二氮嗪 100 μmol/L 预处理组(C 组) ,缺氧+二氮嗪 100 μmol/L+5-羟癸酸 100 μmol/L 预处理组(D 组) ,缺 氧+5-羟癸酸 100 μmol/L 预处理组 (E 组) 缺氧+二氮嗪 100 μmol/L+LY294002 50μmol/L 预处理 , 组(F 组) ,各组神经元每天给予相应药物预处理 1 h,连续 3 d,继而缺氧 4 h 复氧 24 h,观察神经 元的活力,凋亡率,Akt,Bcl-2,Bax 蛋白的表达水平.结果:C 组与 B,D,E 3 组缺氧组比较, 海马神经元的活力增强,凋亡率降低,Akt,Bcl-2 蛋白表达增强,Bax 蛋白表达减弱(P<0.01) ;F 组与 C 组比较,海马神经元的活力降低,凋亡率增高,Akt,Bcl-2 蛋白表达降低,Bax 蛋白表达增 强(P<0.01) .结论:Akt 信号通路参与或部分参与了二氮嗪预处理抗缺氧复氧后大鼠海马神经元凋 亡的作用. 关键词:药物预处理;缺氧耐受性;Akt;Bcl-2;Bax;LY294002 Relation of Akt signal transduction passageway and the mechanism of diazoxide preconditioning for anti-apoptosis in cultured hippocampal neurons by anoxia- reoxygenation in rats Li Jiemeng, Chen Yanqing, Liu Rongguo, Wu Xiaodan. Department of Anaesthesiology, Fujian Provincial Hospital, Fuzhou 350001 CHINA Abstract Objective To investigate relation of Akt signal transduction passageway and the mechanism
    of diazoxide preconditioning for anti-apoptosis in cultured hippocampal neurons by anoxia-reoxygenation in rats. Methods Isolated cultured hippocampal neurons of rat were assigned into the following six groups randomly: control group (Group A), diazoxide 0μmol/L group (Group B), diazoxide 100 μmol/L group (Group C), diazoxide 100 μmol/L and 5-hydroxydecanoate 100 μmol/L group (Group D), 5-hydroxydecanoate 100 μmol/L group (Group E), diazoxide 100 μmol/L and LY294002 50 μmol/L group (Group F). The hippocampal neurons were treated with diazoxide 1 h, per day for 3 days before being subjected to 4 h oxygen deprivation followed by reoxygenation. The neuronal vitality was assayed and apoptosis rate determined after 24 h reoxygenation. The expression of Akt, Bcl-2 and Bax protein was determined by western blotting. Results The vitality of hippocampal neurons in Group C is significant higher than that in Group B, D and E, whereas the apoptotic rate was opposite (P<0.01); Akt, Bcl-2 protein in Group C expressed more intensively than that in Group B, D and E, while Bax protein was weaken (P<0.01). The vitality of hippocampal neurons in Group F is significant lower than that in Group C, whereas the apoptotic rate was opposite (P<0.01); Akt, Bcl-2 protein in Group F expressed significant lower than that in Group C, while Bax protein was strengthen (P<0.01). Conclusions Akt signal transduction passageway completely or partly mediated the process of diazoxide preconditioning for

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