【摘要】 目的 研究亚低温对脑缺血,再灌注(I/R)大鼠脑海马CA1区细胞凋亡及Bcl-2、Bax蛋白表达的影响。方法 采用双侧颈总动脉夹闭加静脉放血再回输法建立全脑I/R模型。24只雄性Wistar大鼠随机分成三组,每组8只。常温非缺血组(Sham组):未建立脑I/R模型,体温正常;常温缺血组(NT组):建立全脑I/R模型,体温正常;亚低温缺血组(HT组),建立全脑I/R模型,体温降至32.5-33.5℃,持续3 h。于再灌注72 h取脑组织,用原位末端标记法测定海马CA1区细胞凋亡、免疫组织化学法检测Bcl-2、Bax蛋白表达。结果 NT组和HT组细胞凋亡率明显多于Sham组(P<0.01),但HT组细胞凋亡率明显少于NT组(P<0.01);NT组和HT组的Bcl-2、Bax蛋白表达高于Sham组(P<0.01),但两组间差异无显著性(P>0.05)。结论 亚低温减少全脑I/R后海马CA1区细胞凋亡,但不改变Bel-2及Bax蛋白表达。更多还原

【Abstract】 Objective To investigate the effects of mild hypothermia (32.5 - 33.5℃) on neuronal cell apoptosis , Bcl-2 and Bax protein expression in hippocampus following global cerebral ischemia-reperfusion (I/R) in rats. Methods Twenty-four male Wistar rats weighing 250-300 g were randomly divided into three groups of 8 animals : (A) control group-normothermia-sham operation; (B) normothermia-global cerebral I/R (N-I/R); (C) hypothermia-global cerebral I/R (H-I/R) . Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP = 40mmHg) induced by exsanguinations. Global cerebral ischemia was confirmed by dilated pupils and EEG. Global cerebral ischemia was maintained for 20 min followed by 72 h reperfusion. Mild hypothermia was induced by alcohol spreyed over the rats combined with fanning and maintained at 32.5-33.51 for 3 h. At the end of 72 h reperfusion the animals were sacrificed and hippocampus was obtained for detection of neuronal cell apoptosis (TUNEL) and Bcl-2 and Bax protein expression (immuno -histochemistry technique) . Results The number of apoptotic neuronal cells increased significantly in group B (N-I/R) and C (H-I/R) compared with that in control group (A) (P < 0.05 or 0.01). There was significantly less number of apoptotic neuronal cells in group C (H-I/R) than in group B (N-I/R) . Bcl-2 and Bax protein expression were significantly increased in group B and C compared with those in control group, but there was no significant difference in Bcl-2 and Bax protein expression between group B and C. Conclusion Mild hypothermia attenuates apoptotic neuronal cell death associated with I/R but does not alter Bcl-2 and Bax protein expression following global cerebral I/R.更多还原