二氮嗪对大鼠脑缺血再灌注损伤保护作用及机制-神经病学专业论文.docxVIP

3 、 Compared with N group, I/R group expressions of caspase-3 enhanced at reperfusion in ischemic region (P0.05). Compared with I/R group, DZ group significantly reduced the expression of caspase- 3 (P0.05) . Conclusion：Mitochondrial k-atp channels opener Diazoxide has potential neuroprotective effect against cerebral ischemia-reperfusion injury in rats. The protective neural function specific mechanisms may and the following aspects about: 1、Improving brain tissue mitochondria the activity of Na+-K+-ATPase、Ca2+-Mg2+-ATPase; Maintaining sodium pumps and calcium pumps stability and the mitochondria ions balance distribution; Reduceing the mitochondrial membrane potentia and the mitochondrial oedema. 2、Enhance the activity of SOD and the ability of scanvenge oxygen free radicals; Reduce the MDA generation and inhibit lipid peroxidation , decrease oxygen free radicals on the neurons damage. 3 、Reduce the expression of caspase-3 in brain ischemia-reperfusion region , prevent cell apoptosis. Key Words: Diazoxide; mitochondria K-ATP sensitive channel; ischemia-reperfusion; Na+-K+-ATPase、Ca2+-Mg2+-ATPase; SOD ; MDA ; Caspase-3. 英文缩略对照 ATP Adenosines triphosphate 三磷酸腺苷 Apaf-1 Apoptosis activating factor-1 凋亡酶活化因子-1 Caspase-3 Cystinylaspartate specific protease 半胱氨酸天冬氨酸蛋白酶-3 CIP Cerebal Ischemic Preconditioning 脑缺血预处理 DZ Diazoxide 二氮嗪 I/R Ischemia-Reperfusion 缺血再灌注 K-ATP K-ATP sensitive channel ATP 敏感性钾通道 MCAO Middle cerebral artery occlusion 大脑中动脉阻断 MDA Malondialdehyde 丙二醛 mitoK-ATP mitochondria K-ATP sensitive channel 线粒体 ATP 敏感性钾通道 SOD Superoxide dismutase 超氧化物歧化酶 K-ATP ATP-sensitive K+ channels ATP 敏感性钾通道 PKA protein kinase A 蛋白激酶 A PKC protein kinase C 蛋白激酶 C ROS Reactive Oxygen Species 活性氧 GluTs glutama tet ransporters 谷氨酸转运体 学位论文独创性声明 本人声明，所呈交的学位论文系在导师指导下本人独立完成的研究成果。文中任何引 用他人的成果，均己做出明确标注或得到许可。论文内容未包含法律意义上已属于他人的 任何形式的研究成果，也不包含本人已用于其他学位申请的论文或成果。与我一同工作的 同志对本研究所做的任何贡献均已在论文中作了明确的说明并表示谢意。 本人如违反上述声明，愿意承担以下责任和后果: 1、交回学校授予的学位证书; 2、学校可在相关媒体上对作者本人的行为进行通报; 3、本人按照学校