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目的研究丁苯酞干预对大鼠脑缺血再灌注损伤后不同时点脑组织中热休克蛋白10(HSP10)表达的影响,并探讨丁苯酞对缺血性脑血管病保护作用的机制。方法采用夹闭双侧颈总动脉的方法制作大鼠前脑缺血再灌注模型;H&E染色和NSE免疫组化染色神经元,观察脑组织的形态变化和记数各组神经元数目;免疫组织化学检测对照组、缺血再灌注组及丁苯酞干预组大鼠脑组织HSP10的表达水平变化。结果脑缺血再灌注后丁苯酞干预组及缺血再灌注组HSP10表达水平于再灌注后6h开始上调,3d达到高峰,丁苯酞干预组各时间点HSP10阳性表达指数均高于缺血再灌注组,丁苯酞干预组脑组织的损伤程度明显轻于脑缺血再灌注组(P<0.05)。结论丁苯酞可能通过上调大鼠缺血再灌注损伤后脑组织HSP10的表达,从而抑制前脑缺血再灌注损伤后细胞凋亡,减少神经元死亡,减轻缺血再灌注后脑组织的损伤。
Objective To investigate the effect of butylphthalide on the expression of heat shock protein 10 (HSP10) in brain tissue at different time points after cerebral ischemia-reperfusion injury in rats and to explore the protective effect of butylphthalide on ischemic cerebrovascular disease. Methods The model of forebrain ischemia-reperfusion was established by occluding bilateral common carotid arteries. The neurons were stained with H & E staining and NSE immunohistochemistry. The morphological changes of brain tissue were observed and the number of neurons in each group was counted. Changes of HSP10 expression in brain tissue of rats in control group, ischemia - reperfusion group and butylphthalide group. Results The expression of HSP10 in butylphthalide group and ischemia-reperfusion group after cerebral ischemia and reperfusion increased at 6h after reperfusion and peaked at 3d, and the HSP10 positive expression index at each time point in butylphthalide group was higher than that in ischemia group In the reperfusion group and the butylphthalide group, the damage of brain tissue in the intervention group was lighter than that in the cerebral ischemia reperfusion group (P <0.05). Conclusion Butylphthalide may inhibit the apoptosis of forebrain after ischemia-reperfusion injury by increasing the expression of HSP10 in rat brain after ischemia-reperfusion injury, reduce neuronal death and reduce the damage of brain tissue after ischemia-reperfusion injury.