论文部分内容阅读
目的:观察莲心碱对大鼠脑缺血/再灌注后TNF-a表达的影响并探讨其作用机制。方法:采用大鼠大脑中动脉线栓(MCAO)法制备局灶性脑缺血/再灌注模型,将90只SD雄性大鼠随机分为3组:假手术组、缺血再灌注组和莲心碱组,应用免疫组化法分别检测各组大鼠缺血/再灌后TNF-a的动态变化并进行图像分析。结果:与假手术组比较,缺血再灌注组大鼠TNF-a的表达于脑缺血/再灌注3h已有明显升高,24h达到高峰。与损伤对照组比较,莲心碱组大鼠TNF-a的表达24h减少。结论:莲心碱的神经保护机制可能与抑制TNF-a的表达有关。
OBJECTIVE: To observe the effect of liensinine on the expression of TNF-a after cerebral ischemia/reperfusion in rats and to explore its mechanism of action. METHODS: Focal cerebral ischemia/reperfusion model was established by middle cerebral artery occlusion (MCAO) in rats. 90 SD male rats were randomly divided into 3 groups: sham operation group, ischemia reperfusion group and lotus heart In the alkaloid group, the dynamic changes of TNF-a after ischemia/reperfusion in each group were detected by immunohistochemistry and image analysis was performed. RESULTS: Compared with the sham-operated group, the expression of TNF-a in the ischemia-reperfusion group was significantly increased at 3 h after cerebral ischemia/reperfusion, and peaked at 24 h. Compared with the injury control group, the expression of TNF-a in the neonicitine group decreased after 24 hours. CONCLUSIONS: The neuroprotective mechanism of serenine may be related to the inhibition of TNF-a expression.