胰岛素样生长因子-1对大鼠局灶性脑缺血再灌注后神经细胞凋亡及Bcl-2,Bax蛋白表达的影响(英文)

Effects of IGF-1 on apoptosis following cerebral ischemia and reperfusion in rats and its mechanism

目的研究胰岛素样生长因子-1(IGF-1)对大鼠局灶性脑缺血再灌注后神经细胞凋亡及Bcl-2,Bax蛋白表达的影响,探讨IGF-1对脑缺血再灌注损伤的保护作用机制。方法制作大鼠大脑中动脉缺血再灌注模型。30只Wistar雄性大鼠被随机分为假手术组、缺血组及IGF-1治疗组。于缺血10min后经尾静脉给予IGF-110μg,应用TTC染色观察梗死灶体积,应用免疫组化染色和TUNEL法检测Bcl-2,Bax蛋白表达及神经凋亡细胞。结果与缺血组比较,IGF-1治疗组梗死体积明显减少(P<0.01),凋亡细胞数明显减少(P<0.01),Bcl-2蛋白表达明显升高(P<0.01),Bax蛋白表达明显降低(P<0.01)。结论IGF-1通过增加Bcl-2蛋白表达,减少Bax蛋白表达,减少神经细胞凋亡,对脑缺血再灌注损伤起保护作用。

Objective: To study the effects of IGF-1 on apoptosis and the expression of Bcl-2 and Bax following cerebral ischemia and reperfusion and evaluate the protecting mechanism of IGF-1. Methods: The model of middle cerebral artery occlusion (MCAO) and reperfusion was set up. Thirty Wistar male rats were randomly divided into sham-operated group, ischemic group and IGF-1 treated group. IGF-1 of 10 μg was injected via caudal vein after 10 minutes with cerebral ischemia. The brain sections were used for TTC staining, TUNEL staining, Bcl-2 and Bax immunohistochemical staining. Results: Compared with ischemic group, the infarct volumes, the number of apoptotic cells and the expression of Bax positive cells in IGF-1 treated group were decreased significantly (P <0.01). The expression of Bcl-2 positive cells was increased significantly (P <0.01). Conclusions: IGF -1 can decrease apoptosis by up-regulating Bcl-2 and down-regulating Bax.