SHH的激活对永久性脑缺血大鼠细胞骨架蛋白α-tubulin、MAP-2表达的影响

The activation of the SHH pathway affects the cytoskeletal proteinα-tubulin and MAP-2 in stroke rat model

目的探讨应用purmorphamine激活SHH信号通路后对大鼠脑缺血区细胞骨架蛋白α-tubulin、MAP-2的影响。方法采用线栓法制备大鼠急性大脑中动脉脑缺血模型,将大鼠随机分为假手术组、模型组和给药组,其中给药组给予purmorphamine腹腔注射。于术后1d、3d、7d、14d用免疫组化法测定脑缺血后不同时相α-tubulin、MAP-2的表达,用RT-PCR测定Gli-1的表达。结果假手术组各时间点α-tubulin、MAP-2、Gli-1的表达差异无统计学意义;与之相比,模型组α-tubulin、MAP-2各时间点含量明显低于假手术组(P<0.05);给药组与模型组比较在1d、3d、7d各时间点α-tubulin、MAP-2的表达明显增多,差异有统计学意义(P<0.05),第14天时趋于稳定;而给药组Gli-1各时间点的表达明显高于假手术组和模型组,差异有统计学意义(P<0.05)。结论激活SHH信号通路可促进缺血区α-tubulin、MAP-2表达增加,这可能是其减轻脑缺血后神经损伤的机制之一。

Objective To explore the effects of activation of the Sonic hedgehog signaling（SHH） pathway on cytoskeletal protein α-tubulin and MAP-2 in rats of cerebral ischemia with purmorphamine.Methods The model of sroke injury in rats was made by middle cerebral artery occlusion.All the rats were randomly divided into three groups： sham group,model group and treatment group,while the treatment group was given intraperitoneal injection of purmorphamine,an specific activator of SHH pathway.At the time point of 1d、3d、7d、14d after cerebral ischemia,the expression of α-tubulin and MAP-2 in rats was detected by immunohistochemistry,and the expression of Gli-1 was observed by RT-PCR.Results The expression of the parameters in sham group on every time point has no difference with others,while,the expression of α-tubulin and MAP-2 of the model group was lower than those of the sham group.The expression level of α-tubulin,MAP-2 was higher in treatment group at the time of 1d、3d、7d than in model group（P 0.05）;and the expression of Gli-1 on every time point in the treatment one was higher than the sham one and the model one.Conclusion The activation of the SHH pathway in cerebral ischemia could increase the expression of α-tubulin and MAP-2,which maight be one of the mechanism to reduce the stroke damage after ischemia.