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神经节苷酯GM1对脑缺血后热休克蛋白70表达的影响
引用本文:王云甫,钟建新,黄朝芬,何国厚.神经节苷酯GM1对脑缺血后热休克蛋白70表达的影响[J].中国现代医学杂志,2003,13(2):19-20,23.
作者姓名:王云甫  钟建新  黄朝芬  何国厚
作者单位:湖北省郧阳医学院附属太和医院神经科,十堰,442000
摘    要: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。

关 键 词:脑缺血  神经节苷酯  热休克蛋白70  动物实验

EFFECT OF MONOSIALOGANGLIOSIES ON THE EXPRESSION OF HEAT SHOCK PROTEIN 70 IN RATS WITH FOCAL CEREBRAL ISCHEMIA
Wang Yunfu,Zhong Jianxin,Huang Chaofen,et al..EFFECT OF MONOSIALOGANGLIOSIES ON THE EXPRESSION OF HEAT SHOCK PROTEIN 70 IN RATS WITH FOCAL CEREBRAL ISCHEMIA[J].China Journal of Modern Medicine,2003,13(2):19-20,23.
Authors:Wang Yunfu  Zhong Jianxin  Huang Chaofen  
Institution:Wang Yunfu,Zhong Jianxin,Huang Chaofen,et al. Department of Neurology,Taihe Hospital of Yunyang Medical College,Shiyan 44200
Abstract:Objective:To investigate the effect of monosialo-gangliosides (GM1) on brain injury and the expression of heat shock protein 70 (HSP70) in experimental reversible middle cerebral artery occlusion(MCAO).Methods:Reversible MCAO rats were induced with the use of intraluminal suture occlusion method created by Koizumi. 32 male Wistar rats were divided randomly into 4 groups: A)Normal group, B) MCAO group, C) MCAO + normal saline(NS) group, D) MCAO +GM1 group (GM1 20mg/kg in saline solution) . The different drugs were adiministered intraperitoneally after MCAO 2 hours in group C and D. The rats were sacrificed on 5th day after MCAO. Then Nissl staining and HSP70 immunocytochemistry were performed. The numerial density (ND) of all positive neurons were measured by CMIAS image analysis system.And the data were analyzed by SPSS 10.0 statistical software.Results:The numerial density(ND) of Nissl staining neuron in hippocampal were markedly decreased after MCAO, especially in hippocampal CA1; with the treatment of GM1, neuronal loss was greatly alleviated. MCAO induced the expression of HSPTO, the positive neurons were found in cortex and hippocampal; and the ND of HSPTO positive neurons were greatly reduced after the GM1 therapy.Conclusion:The study suggested GM1 could attenuate brain damage after cerebral ischemia, and inhibiting the HSP70 expression might be one of the treatment mechanism.
Keywords:Cerebral Ischemia  Neuroprotection  Monosialo-Gangliosides  Heat Shock Protein 70  Rat
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