姜黄素通过PI3K/AKT信号通路减轻幽门螺杆菌感染小鼠胃黏膜炎症反应及氧化应激

Curcumin attenuates gastric mucosal inflammatory response and oxidative stress in helicobacter pylori-infected mice via PI3K/AKT signaling pathway

目的探讨姜黄素对幽门螺杆菌感染小鼠胃黏膜炎症反应及氧化应激的影响及可能机制。方法30只雄性BALB/C小鼠随机分为空白组(Control)、感染组(Infection)与姜黄素组(Curcumin),每组10只。HE染色检测各组小鼠胃黏膜病理形态学改变;qRT-PCR检测各组小鼠胃黏膜组织中16s rRNA、SS1、ureA以及SSA mRNA的水平;ELISA检测各组小鼠血清中SOD、CAT、MDA、IL-1β、IL-8和TNF-α含量;Western-blot检测小鼠胃黏膜组织p-PI3K、PI3K、AKT与p-AKT蛋白的表达。结果幽门螺杆菌感染小鼠模型中胃黏膜炎症损伤程度、毒力因子表达水平、血清炎症反应和氧化应激反应、p-PI3K和p-AKT表达水平显著高于对照组。姜黄素可降低幽门螺杆菌感染小鼠胃黏膜炎症反应,抑制幽门螺杆菌毒力反应、氧化应激水平;下调小鼠胃黏膜组织p-PI3K和p-AKT蛋白表达水平。结论姜黄素可通过抑制PI3K/AKT信号通路减轻幽门螺杆菌感染小鼠胃黏膜炎症反应及氧化应激。

Objective To investigate the effects of curcumin on gastric mucosal inflammation and oxidative stress in Helicobacter pylori infected mice and its possible mechanism.Methods Thirty male BALB/C mice were randomly divided into control group,infection group and curcumin group,with 10 mice in each group.The pathological changes of gastric mucosa were detected by HE staining.The levels of 16s rRNA,SS1,ureA and SSA mRNA in gastric mucosa were detected by qRT-PCR.The levels of SOD,CAT,MDA,IL-1β,IL-8 and TNF-α in serum were detected by ELISA.The expressions of p-PI3K,PI3K,AKT and p-AKT were detected by Western blot.Results The degree of inflammatory damage in gastric mucosa,the expression levels of virulence factors,inflammatory response in serum and oxidative stress,and the expressions of p-PI3K and p-AKT in H.pylori-infected mice models were significantly higher than those in the control group.Curcumin reduced inflammatory response and inhibits oxidative stress in the gastric mucosa of helicobacter pylori-infected mice,down-regulated the expressions of p-PI3K and p-AKT.Conclusion Curcumin could reduce gastric mucosal inflammation and oxidative stress in H.pylori infected mice by inhibiting PI3K/AKT signaling pathway.