PI3K通路发挥抗氧化应激在大鼠脑缺血/再灌注损伤保护机制探讨  

The protective mechanism of PI3K pathway against oxidative stress in cerebral ischemia/reperfusion injury inrats

作　　者：蒲天强 刘树改 龙燕玲[1] 梁秋霞 刘宏[1] Pu Tianqiang;Liu Shugai;Long Yaning;Liang Qiuxia;Liu Hong(Cerebrovascular Disease Department,Guangyuan Central Hospital,Guangyuan Sichuan 628000,China)

机构地区：[1]广元市中心医院脑血管病科,四川628000

出　　处：《脑与神经疾病杂志》2023年第11期678-682,共5页Journal of Brain and Nervous Diseases

基　　金：2019年四川省医学科研课题(S19006)。

摘　　要：目的 本研究分析磷脂酰肌醇-3激酶(PI3K)通路发挥抗氧化应激在大鼠脑缺血/再灌注(I/R)损伤保护机制;方法 喂养SD大鼠,制作脑I/R损伤模型,然后随机分为非抑制剂组、低剂量抑制剂组和高剂量抑制剂组3组,分别于持续给药7 d之后、14 d之后处死各组大鼠7只和8只,对其脑部组织进行提取,分析和比较不同组别大鼠脑组织中抗氧化酶活性及PI3K激酶、一氧化氮(NO)、B淋巴细胞瘤-2 (bcL-2)基因、磷酸化蛋白激酶B (P-AKt)的表达量。结果 发现给药前,三组的丙二醛(MDA)、化学需氧量(COD)的表达量无明显差异(P> 0.05),不同剂量的两组抑制剂组,MDA、COD的表达量明显高于给药前,且高剂量组比低剂量组的MDA、COD的表达更高(P<0.05);而非抑制剂组,在前后MDA、COD的表达量无明显改变(P>0.05)。给药后,高剂量组和低剂量组PI3K、NO、Bcl-2、p-Akt与非抑制剂组比,表达比较差异有统计学意义,且高剂量组与低剂量组之间比较差异有统计学意义(P <0.05)。结论 通过抑制剂方法I/R损伤的大脑中,可能通过抑制PI3K通路来减少脑血管细胞的氧化损伤,从而起到对脑I/R损伤进行保护的作用。Objective To investigate the protective mechanism of PI3K pathway against oxidative stress in cerebral ischemia/reperfusion injury in rats.Methods SD rats were fed and the cerebral ischemia/reperfusion injury model was made.Then 7 and 8 rats in each group were sacrificed after 7 and 14 days of continuous administration,respectively,and their brain tissues were extracted.The activities of antioxidant enzymes and the expressions of phosphatidylinositol-3 kinase,nitric oxide,B-lymphocytoma-2 gene and phosphorylated protein kinase B in brain tissues of rats in dfferent groups were analyzed and compared.Results The modeling rate was 90%.The remaining 45 rats were divided into groups,and the activities of antioxidant enzymes in brain cells were compared before and after administration.It was found that the expression levels of MDA and COD(unchanged Chinese)were not significantly different among the three groups before administration(P>O.05),the expressions of MDA and COD in the two inhibitor groups with different doses were significantly higher than before,and the expressions of MDA and COD in the high-dose group were higher than those in the low-dose group(P<O.05);In the non-inhibitor group,MDA and COD expression levels did not change significantly(P>0.05).After administration,the expressions of PI3K,NO,Bcl-2,p-Akt in high-dose and low-dose groups were significantly different from those in non-inhibitor groups,and there were also differences between high-dose and low-dose groups(P<0.05).Conclusion Ingestion of inhibitors into the brain with ischemia/reperfusion injury may reduce oxidative damage of cerebrovascular cells by inhibiting PI3K pathway,thus playing a protective role against cerebral ischemia/reperfusion injury.

关 键 词：磷脂酰肌醇-3激酶 抗氧化应激 大鼠实验 脑缺血/再灌注损伤 

分 类 号：R651.1[医药卫生—外科学]