全脑缺血再灌注损伤后ERK在大鼠海马的表达及热休克预处理对其表达的影响
脑缺血;再灌注损伤;热休克预处理;细胞外信号调节MAP激酶类,,脑缺血;再灌注损伤;热休克预处理;细胞外信号调节MAP激酶类,全脑缺血再灌注损伤后ERK在大鼠海马的表达及热休克预处理对其表达的影
Expression of ERK in rat hippocampus after global cerebral ischemia/reperfusion and effect of heat shock preconditioning on itL JianRui, MA HongZhong, XUE RongLiang
Department of Anesthesiology, Second Affiliated Hospital, Medical College, Xian Jiaotong University, Xian 710004, China
【Abstract】 AIM: To investigate the expression of ERK in hippocampus of SD rats after global cerebral ischemia/reperfusion and the effect of heat shock preconditioning on it, and to clarify the role of ERK in global cerebral ischemia/reperfusion injury. METHODS: Ninety healthy male SD rats were divided into 3 groups randomly: sham operation group (SO group, n=30), ischemia/reperfusion group (IR group, n=30) and heat shock preconditioning group (HSP group, n=30). Global cerebral ischemia/reperfusion model was produced by 4VO method. The rats were put in 42℃ for 15 min as heat shock preconditioning, then subjected to 6 min ischemia followed by 2, 6, 12, 24 h, 3, 5 d reperfusion, and all rats were executed at corresponding time points. HE staining, immunohistochemical staining and TUNEL staining of brain tissue section were performed. RESULTS: In CA1 of IR group, ERK was expressed 2 h after global cerebral ischemia/reperfusion, peaked at 24 h and still lasted at 5 d. Expression in CA3 was weaker than that in CA1 and cellular damage in CA1 was more obvious. Expression of ERK in CA1 and CA3 of HSP group were weaker than that in IR group at each time points (P<0.05). At the same time, cellular damage was weaker and apoptotic cells decreased(P<0.05). CONCLUSION: Overexpression of ERK after global cerebral ischemia/reperfusion participated in the neuronal injury procedure and heat shock preconditioning exerted its brain protective function through its suppressive effect on the overexpression of ERK. ......
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