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目的:探讨阿司匹林(ASA)对大鼠脑缺血后解偶联蛋白-4(UCP-4)和ATPase-6表达的影响。方法:采用线栓法在血管内堵塞右侧大脑中动脉起始部2 h,制作大脑中动脉支配区缺血模型。随机分为对照组和ASA组(腹腔注射ASA80 mg·kg-1.d-1),每组按再灌注时间0、6、24、48和72 h分为5个亚组。采用间接免疫荧光方法检测UCP-4和ATPase-6表达。结果:UCP-4在缺血后6 h表达增加(P<0.05),随后表达下降,72 h达最低(P<0.01);ATPase-6在缺血6 h后呈下降趋势。与对照组比较,ASA干预后,缺血边缘区UCP-4表达增加,缺血后48 h最为显著(P<0.01);ATPase-6表达下降幅度减少,缺血24 h时最为明显(P<0.01)。结论:ASA增加缺血脑组织线粒体内UCP-4和ATPase-6的表达是其神经保护作用机制之一。
Objective: To investigate the effect of aspirin (ASA) on the expression of uncoupling protein-4 (UCP-4) and ATPase-6 after cerebral ischemia in rats. Methods: The artery occlusion of the right middle cerebral artery at the beginning of 2 h was performed by using the suture method to make the middle cerebral artery dominant area ischemia model. Randomly divided into control group and ASA group (intraperitoneal injection of ASA 80 mg · kg-1.d-1), each group according to reperfusion time 0,6,24,48 and 72 h divided into five subgroups. Indirect immunofluorescence was used to detect the expression of UCP-4 and ATPase-6. Results: The expression of UCP-4 increased at 6 h after ischemia (P <0.05), and then decreased at 72 h (P <0.01). The level of ATPase-6 decreased after 6 h of ischemia. Compared with the control group, the expression of UCP-4 in ischemic border area increased after ASA intervention, and the expression of UCP-4 was the highest at 48 h after ischemia (P <0.01). The decrease of ATPase-6 expression was the most significant at 24 h after ischemia (P < 0.01). CONCLUSION: ASA can increase the expression of UCP-4 and ATPase-6 in mitochondria of ischemic brain tissue, which is one of the mechanisms of neuroprotection.