【摘要】 目的:探究阿司匹林对缺血性脑梗死大鼠神经元细胞凋亡的影响及其机制。方法:90只健康SD大鼠随机分为3组,分别为对照组、模型组、阿司匹林组(50 mg·kg^-1),每组各30例,除对照组外,其余两组均采用颈总动脉阻断的方法建立大鼠缺血性脑梗死模型。阿司匹林组造模前5天连续给予50 mg·kg^-1剂量的阿司匹林灌胃,第6日处死3组大鼠,TUNEL法检测大鼠脑组织神经元细胞凋亡情况;Western blot技术检测大鼠脑组织神经元Bcl-2、Bax蛋白表达及Cyt-C释放情况。结果:TUNEL法检测结果显示阿司匹林组大鼠脑组织神经元细胞凋亡率明显少于模型组,Western blot技术检测结果显示阿司匹林组大鼠脑组织神经元Bcl-2蛋白表达量显著高于模型组,而Bax蛋白表达及Cyt-C释放量显著低于模型组,以上差异均具有统计学意义（P<0.05）。结论:阿司匹林能够有效减轻因缺血性脑梗死引发的脑组织神经元细胞凋亡从而发挥神经保护作用,其机制可能与减少线粒体Cyt-C释放,同时升高Bcl-2蛋白表达量以及降低Bax蛋白表达量有关。更多还原

【Abstract】 Objective:To explore the effect of aspirin on neuronal apoptosis and its mechanism in rats with ischemic cerebral infarction. Methods:90 healthy SD rats were randomly divided into 3 groups,named the control group,the model group,and the aspirin group(50 mg·kg^-1),each group with 30 cases. Except for the control group,the other two groups were treated with common carotid artery obstruction. To establish a rat model of ischemic cerebral infarction. The aspirin group was given continuous intragastric administration of aspirin at a dose of 50 mg·kg^-1 5 days before modeling. On the 6 th day,3 groups of rats were sacrificed. The TdT-mediated dUTP Nick-End Labeling（TUNEL） method was used to detect neuronal cell apoptosis in rat brain tissue. Western blot technology was used to detect rat brain tissue nerve. The expression of B-cell lymphoma-2（Bcl-2） and Bcl2-associated X（Bax） protein in metabolites and the release of Cyt-C. Results:The TUNEL method showed that the apoptosis rate of neuronal cells in the brain tissue of the aspirin group was significantly lower than that of the model group. The results of Western blot technology showed that the expression of Bcl-2 protein in the brain tissue of the aspirin group was significantly higher than that of the model group. The Bax protein expression and cytochrome C（Cyt-C） release amount were significantly lower than the model group,and the above differences were statistically significant（P<0.05）. Conclusion:Aspirin can effectively reduce the neuronal cell apoptosis in brain tissue caused by ischemic cerebral infarction and play a neuroprotective effect. The mechanism may be related to reducing the release of mitochondrial Cyt-C,while increasing the expression of Bcl-2 protein and reducing Bax. The amount of protein expression is related.更多还原