普拉格雷干预对脑梗死大鼠神经功能的影响及可能机制

发布时间：2018-07-05 15:46

本文选题：普拉格雷 + 脑梗死　；参考：《中国老年学杂志》2017年24期

【摘要】：目的考察普拉格雷对脑梗死大鼠神经功能的影响及可能机制。方法雄性SD大鼠随机分为假手术组,模型组和普拉格雷组3组,每组40只。假手术组与模型组灌胃给予生理盐水,普拉格雷组给予普拉格雷10 mg·kg~(-1)·d~(-1),连续给药14 d。记录或检测各组行为障碍、组织病理学改变、脑内半胱天冬酶(Caspase)-3及程序化死亡基因(PDCD)-5表达情况,外周血超氧化物歧化酶(SOD)、丙二醛(MDA)、神经元特异性烯醇化酶(NSE)及S-100β蛋白表达情况。结果与假手术组比,模型组及普拉格雷组神经功能评分升高显著(P0.05);与模型组比较,普拉格雷组神经功能评分显著降低(P0.05)。假手术组脑组织细胞结构完整;模型组细胞排列紊乱,水肿严重,血管充血;与模型组比较,普拉格雷组脑组织结构较完整,且坏死及水肿程度降低。与假手术组比,模型组可见大量Caspase-3和PDCD-5细胞(P0.05),SOD明显降低(P0.05),MDA、NSE和S-100β明显增高(P0.05);与模型组比,普拉格雷组Caspase-3和PDCD-5细胞显著降低(P0.05),SOD明显增高(P0.05),MDA、NSE和S-100β明显降低(P0.05)。结论普拉格雷可以通过抑制Caspase-3及PDCD-5凋亡因子,调控SOD、MDA、NSE及S-100β表达从而改善脑梗死大鼠的神经功能障碍。
[Abstract]:Objective to investigate the effect and possible mechanism of prasgore on the neural function of cerebral infarction rats. Methods male SD rats were randomly divided into sham operation group, model group and pragre group 3 groups, 40 rats in each group. The sham operation group and model group were given saline for gastric perfusion, and pragre group was given prasgore 10 mg. Kg~ (-1) d~ (-1), and a continuous dose of 14 d. was recorded or The expression of Caspase -3 and programmed death gene (PDCD) -5, peripheral blood superoxide dismutase (SOD), malondialdehyde (MDA), neuron specific enolase (NSE) and S-100 beta egg white expression were detected in each group of behavioral disorders, histopathological changes, -3 and programmed death gene (PDCD), and the results were compared with the sham group, model group and prasgore group The function score increased significantly (P0.05). Compared with the model group, the nerve function score of the prasug group was significantly reduced (P0.05). The cell structure of the brain tissue in the sham operation group was complete, the model group was disorganized, the edema was serious, and the blood vessels were congested; and the brain tissue of the prasug group was more complete and the necrosis and edema decreased. A large number of Caspase-3 and PDCD-5 cells (P0.05) were found in the model group, and the SOD decreased significantly (P0.05), MDA, NSE and S-100 beta were significantly increased (P0.05), and the Caspase-3 and PDCD-5 cells in the prasgore group were significantly lower than those in the model group. Se-3 and PDCD-5 apoptotic factors regulate the expression of SOD, MDA, NSE and S-100 beta, thereby improving neurological deficits in rats with cerebral infarction.
【作者单位】：武警浙江省总队杭州医院康复中心;
【基金】：浙江省自然科学基金资助项目(No.LY12H09006)
【分类号】：R743.33

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