黄芪注射液对脑缺血再灌注损伤大鼠脑内血管新生及HIF-1α/VEGF信号转导通路的影响

    Effect of astragalus injection on the angiogenesis and HIF-1α/VEGF signal pathway in brain tissue of rats with cerebral ischemia reperfusion injury

    • 摘要: 目的:探究黄芪注射液对脑缺血再灌注损伤大鼠脑内血管新生及缺氧诱导生长因子-1α(hypoxia inducible factor-1α,HIF-1α)/血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)信号转导通路的影响。方法:72只大鼠随机分为对照组、模型组和黄芪注射液组,每组24只,线栓法复制脑缺血再灌注损伤大鼠模型,评价术前、术后、给药7 d后的神经功能评分,免疫组化法检测脑缺血再灌注损伤皮质微血管密度,RT-PCR法检测脑缺血再灌注损伤皮质HIF-1α mRNA和VEGF mRNA,Western Blotting法检测脑缺血再灌注损伤皮质HIF-1α和VEGF的蛋白表达。结果:给药7d后黄芪注射液组神经功能评分明显低于模型组(P<0.01),微血管密度、HIF-1α mRNA和VEGF mRNA表达水平、HIF-1α和VEGF蛋白表达水平均高于模型组(P<0.01)。结论:黄芪注射液促进脑缺血再灌注损伤大鼠脑内血管新生,其作用机制可能为激活HIF-1α/VEGF信号转导通路。

       

      Abstract: Objective:To explore the effects of astragalus injection on the angiogenesis and HIF-1α/VEGF(hypoxia inducible factors-1α/vascular endothelial growth factor) signal pathway in brain tissue of rats with cerebral ischemia reperfusion injury.Methods:Seventy-two rats were randomly divided into the control group,model group and astragalus injection group(24 rats each group).The rat model of cerebral ischemia reperfusion injury models were established by nylon monofilament induced method.Before operation,after operation and after 7 days of adminstration,the neurological scores in all rats were evaluated,and the expression levels of microvessel density(MVD) in brain tissue of rats were detected by immunohistochemical method,the mRNA and protein expression levels of HIF-1α and VEGF in brain tissue of rats were detected by RT-PCR and Western Blotting,respectively.Results:After 7 dyas of adminstration,the neurological score in astragalus injection group was significantly higher than that in model group(P<0.01),and the level of MVD,mRNA and protein expression levels of HIF-1α and VEGF in astragalus injection group were significantly higher than those in model group(P<0.01).Conclusions:Astragalus injection can promote the angiogenesis in brain tissue of rats with cerebral ischemia reperfusion injury,the mechanism of which maybe activate the pathway of HIF-1α/VEGF.

       

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