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作 者:张伟华[1] 傅松滨[2] 吴博[1] 龚冬梅[3] 赵雅君[1] 李全凤[1] 张力[1] 徐长庆[1]
机构地区:[1]哈尔滨医科大学病理生理学教研室,150081 [2]哈尔滨医科大学遗传学教研室,150081 [3]哈尔滨医科大学药理教研室,150081
出 处:《中国地方病学杂志》2007年第4期364-366,共3页Chinese Jouranl of Endemiology
基 金:国家自然科学基金(30370577);哈尔滨医科大学校青年基金(060015)
摘 要:目的 探讨钙敏感受体(CaSR)参与心肌缺血再灌注损伤诱发细胞凋亡的机制。方法 采用离体大鼠心肌缺血再灌注损伤模型。实验分5组:对照组灌注2h;缺血组单纯缺血40min;缺血再灌注组缺血40min再灌注2h;激动剂组同缺血再灌注组,在再灌注液中加入氯化钆(GdCl3);阻断剂组同缺血再灌注组,在再灌注液中加入氯化镍(NiCl2)和氯化镉(CdCl2)。利用光镜观察各组心肌细胞凋亡情况;检测各组乳酸脱氢酶(LDH)活力和丙二醛(MDA)水平变化;Western Blot分析各组心肌组织中CaSR、Bcl-2和Caspase-3的表达。结果 缺血再灌注和激动剂组细胞凋亡指数、LDH活力和MDA水平明显高于对照组;同时CaSR、细胞浆中的Caspase-3表达也明显高于对照组.反之,Bcl-2表达低于对照组。结论 CaSR参与缺血再灌注损伤所诱发的细胞凋亡。Objective To discuss the mechanism of calcium sensing receptor(CaSR) involved in apoptosis induced in ischemia/reperfusion (I/R). Methods Primary animal models were divided into five groups: (1)Sham control: hearts were continuously perfused for 2 h. (2)Ischemic group: hearts were exposed to 40 min of global ischemia. (3)Ischemia/reperfusion group (I/R group) : hearts were exposed to 40 min of global ischemia, and then reperfused for 2 h. (4)GdCl3, NiCl2, CdCl2-reperfusion group: GdCl3, NiCl2 and CdCl2 were added to KH solution at the beginning of reperfusion after ischemia. (5)NiCl2, CdCl2-reperfusion group: NiCl2 and CdCl2 were added to KH solution at the beginning of reperfusion after ischemia. The morphological changes were observed under optical microscope, the activity of LDH and the content of MDA were determined and the expressions of CaSR, Bcl-2 and Caspase-3 in each group were analyzed using Western Blot. Results The apoptosis index, the activity of LDH, the content of MDA and quantitative expressions of CaSR, and Caspase-3 in I/R and activator groups were significantly higher than those in control group, while Bcl-2 expression was lower than that in control group. Conclusion These data suggest that CaSR is involved in the induction of cardiomyocyte apoptosis during ischemia/reperfusion.
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