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目的研究骨髓基质细胞(BMSCs)对脑缺血治疗作用和机制。方法采用线栓法建立大鼠大脑中动脉缺血模型。对照组和实验组于建模成功后24 h分别经尾静脉注入等体积的PBS液和已制备好的同种异体BMSCs悬液。脑缺血治疗后1、3、7、14、28 d时行神经功能缺损评分;TTC染色、HE染色判断病变的范围及病理改变;采用免疫组化染色检测各时间点脑组织Bc l-2、Bax蛋白的表达。结果与对照组比较,在移植后3、7、14、28 d,实验组大鼠神经功能缺损评分、梗死体积及Bax蛋白表达明显降低(P<0.05),Bc l-2蛋白表达明显升高(P<0.05)。结论经静脉途径移植BMSCs可显著促进脑缺血梗死大鼠的神经功能恢复,缩小梗死体积;通过上调Bc l-2蛋白表达、下调Bax蛋白表达,减少神经细胞凋亡可能是其主要机制之一。
Objective To study the therapeutic effect and mechanism of bone marrow stromal cells (BMSCs) on cerebral ischemia. Methods The rat middle cerebral artery occlusion model was established by thread occlusion. The control group and the experimental group were injected with equal volume of PBS solution and prepared allogeneic BMSCs suspension through the tail vein 24 h after successful modeling. Neurological deficit scores were evaluated at 1, 3, 7, 14, and 28 days after cerebral ischemia. TTC staining and HE staining were used to determine the extent of the lesions and pathological changes. Immunohistochemical staining was used to detect the expression of Bcl-2 , Bax protein expression. Results Compared with the control group, at 3, 7, 14 and 28 days after transplantation, the neurological deficit score, infarct volume and Bax protein expression in the experimental group were significantly decreased (P <0.05), while the Bcl-2 protein expression was significantly increased (P <0.05). Conclusion Transplantation of BMSCs by intravenous route can significantly promote the recovery of neurological function and reduce the infarct volume in rats with cerebral infarction. It may be one of the main mechanisms by up-regulating the expression of Bcl-2, decreasing the expression of Bax protein and decreasing the apoptosis of nerve cells .