大车前苷通过PI3K/Akt信号通路减轻大鼠肠缺血再灌注损伤

Plantamajoside alleviated ischemia reperfusion injury in rats by PI3K/Akt signal pathway

目的探讨大车前苷通过PI3K/Akt信号通路减轻肠缺血再灌注损伤大鼠细胞凋亡的作用及机制。方法 24只SD大鼠随机分为正常对照组、缺血再灌注损伤组与大车前苷组,每组8只,在建模后大车前苷组灌胃给予大车前苷0.4g/kg。各组于再灌注3 h后,通过湿干重检测肠组织含水率;HE染色检测各组肠组织损伤情况;Western blot检测肠组织Bad和Bcl-XL凋亡相关蛋白表达;RT-PCR检测大鼠肠PI3K和Akt mRNA表达情况;Western blot检测肠组织PI3K和Akt蛋白表达。结果与对照组相比,肠缺血再灌注后组织含水率均明显升高,凋亡相关蛋白bad表达上调,Bcl-XL蛋白水平降低,PI3K和Akt mRNA和蛋白表达升高(P<0.05);与损伤组相比,大车前苷干预后肠组织含水率显著降低,凋亡相关蛋白Bad表达下调,Bcl-XL蛋白表达上调;PI3K和Akt mRNA和蛋白表达降低(P<0.05)。结论大车前苷明显减轻肠缺血再灌注损伤,其机制可能与通过PI3K/Akt信号通路调节大鼠细胞凋亡有关。

Objective To investigate the role and mechanism of plantamajoside on intestinal ischemiareperfusion injury in rats. Methods Twenty-four SD rats were randomly divided into three groups(the normal control group;the ischemia-reperfusion injury group;and the plantamajoside group). After surgery, the plantamajoside group was treated with plantamajoside in a dose of 0.4 g/kg. HE staining was used to detect the intestinal tissue damage;Western blot was used to detect the expression of Bad and Bcl-XL;RT-PCR was used to detect the level of PI3 K mRNA and Akt mRNA;Western blot was used to detect the expression of PI3 K and Akt. Results Compared with the control group, the water content of intestinal tissue was significantly increased, the expression of Bad was up-regulated, the level of Bcl XL was decreased, and the mRNA and protein expressions of PI3 K and Akt were increased(P<0.05). Compared with the injury group, the water content of intestinal tissue was significantly decreased, the expression of Bad was down regulated, and the expression of Bcl XL was up-regulated;The expression of mRNA and protein of PI3 K and Akt were decreased(P<0.05). Conclusion Plantamajoside regulated the intestinal ischemia-reperfusion injury in rats, and the mechanism may be related to the regulation of PI3 K/Akt signaling pathway.