论文部分内容阅读
目的 :探讨神经节苷酯GM1对脑缺血后的脑保护作用及其对脑缺血后热休克蛋白 70表达的影响。方法 :采用Koizumi’s线栓法制作可复流大脑中动脉闭塞大鼠模型。 32只雄性、健康Wistar大鼠随机分为正常组、MCAO组、生理盐水对照组、神经节苷酯GM1治疗组。MCAO后第 5天处死动物 ,取脑组织进行Nissl染色及HSP70免疫组化检测。检测结果经CMIAS图像分析系统进行定量分析。结果 :神经节苷酯GM1治疗组组海马各区神经元损伤轻 ,神经元脱失相对较少 ;MCAO后海马各区及大脑皮层均有不同程度的HSP70阳性细胞表达 ,GM1治疗后 ,海马各区及大脑皮层HSP70阳性细胞的数密度值较MCAO组减少。结论 :GM1能减轻脑缺血后的神经元损伤 ,具有脑保护作用 ;抑制HSP70的表达亦可能是神经节苷酯GM1的脑保护作用机制之一。
Objective: To investigate the protective effect of ganglioside GM1 on cerebral ischemia and its effect on the expression of heat shock protein 70 after cerebral ischemia. Methods: Koizumi’s suture method was used to make reperfusion model of middle cerebral artery occlusion in rats. Twenty-two male and healthy Wistar rats were randomly divided into normal group, MCAO group, saline control group and ganglioside GM1 treatment group. Animals were sacrificed on day 5 after MCAO, and brain tissue was taken for Nissl staining and HSP70 immunohistochemistry. The test results were quantitatively analyzed by CMIAS image analysis system. Results: Neurons in the ganglioside GM1 treatment group were lighter in damage and less in neurons. After MCAO, hippocampus and cerebral cortex all expressed HSP70-positive cells in varying degrees. After GM1 treatment, hippocampus and brain The number density of cortical HSP70 positive cells decreased compared with MCAO group. CONCLUSION: GM1 can attenuate the neuronal damage after cerebral ischemia and has neuroprotective effect. Inhibiting the expression of HSP70 may also be one of the protective mechanisms of ganglioside GM1.