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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 investigate the effects of insulin-like growth factor-1 (IGF-1) on neuronal apoptosis and the expression of Bcl-2 and Bax after focal cerebral ischemia-reperfusion in rats and to investigate the effect of IGF-1 on cerebral ischemia-reperfusion Protective mechanism of injury. Methods Rat middle cerebral artery ischemia-reperfusion model was made. Thirty Wistar male rats were randomly divided into sham operation group, ischemia group and IGF-1 treatment group. After 10 min of ischemia, IGF-110 μg was given via the tail vein. The volume of infarction was observed by TTC staining. The expression of Bcl-2, Bax protein and neuronal apoptotic cells were detected by immunohistochemistry and TUNEL. Results Compared with the ischemia group, the infarct volume of the IGF-1 treatment group was significantly decreased (P <0.01), the number of apoptotic cells was significantly decreased (P <0.01), the expression of Bcl-2 protein was significantly increased The expression was significantly decreased (P <0.01). Conclusion IGF-1 can protect cerebral ischemia-reperfusion injury by increasing the expression of Bcl-2 protein, decreasing the expression of Bax protein, decreasing the apoptosis of nerve cells.