双去甲氧基姜黄素通过PI3K/AKT信号通路抑制DSS诱导的溃疡性结肠炎小鼠炎症反应

Bisdemethoxycurcumin suppresses DSS-induced inflammatory response in ulcerative colitis mice via the PI3K/AKT signaling pathway

目的利用DSS诱导的溃疡性结肠炎模型探讨双去甲氧基姜黄素对溃疡性结肠炎的炎症反应的调控及其与PI3K/AKT信号通路的相关性。方法6~8周龄雄性C57BL/6J小鼠18只,分为正常组,模型组,双去甲氧基姜黄素(50 mg/kg)。观察各组小鼠的临床表现、体重及生存时间情况;HE染色观察各组小鼠结肠组织病理损伤情况;QPCR方法检测各组小鼠结肠组织相关炎症因子TNF-α,IL-1β,IL-6,MCP-1的表达水平。WB方法检测各组小鼠结肠组织p-P13K,P13K,p-AKT,AKT蛋白的表达水平。结果与模型组相比,双去甲氧基姜黄素干预组体重下降明显减轻,生存时间延长;HE染色显示与模型组对比,双去甲氧基姜黄素干预组炎性浸润细胞减少,腺体结构较完整;QPCR结果显示与模型组相比,双去甲氧基姜黄素干预组炎症因子TNF-α,IL-1β,IL-6,MCP-1的表达水平明显下降。WB结果显示,与模型组比较,双去甲氧基姜黄素干预组小鼠结肠组织p-P13K,p-AKT蛋白表达水平下降,P13K,AKT蛋白表达水平无明显差异。结论双去甲氧基姜黄素可能通抑制PI3K/AKT信号通路,减轻DSS诱导的小鼠UC的炎症反应。

Objective The modulation of bisdemethoxycurcumin in ulcerative colitis and its relationship to PI3K/AKT signaling pathway were examined using a DSS-induced ulcerative colitis model.Methods Eighteen male C57BL/6J mice at 6-8 weeks of age were divided into normal group,model group,and bisdemethoxycurcumin group(50 mg/kg).The clinical feature,changes of body weight and survival time of each group were observed.Histopathological damage to the colon of mice in each group was observed by HE staining.QPCR assay was applied to detect the expression levels of inflammatory factors TNF-α,IL-1β,IL-6,MCP-1.The expression levels of p-P13K,P13K,p-AKT and AKT in colon tissue of each group were detected by WB.Results Compared with the model group,the bisdemethoxycurcumin intervention group significantly reduced weight loss and prolonged survival time.HE staining showed fewer inflammatory cells and more intact glandular structures in the bisdemethoxycurcumin intervention group compared to the model group.The QPCR results showed that the expression levels of inflammatory factors TNF-α,IL-1β,IL-6 and MCP-1 were significantly decreased in the bisdemethoxycurcumin intervention group compared with the model group.WB results showed that compared with the model group,the expression level of p-P13K and p-AKT in colon tissue of mice in the bisdemethoxycurcumin intervention group was decreased,while the expression level of P13K and AKT was not significantly different.Conclusion Bisdemethoxycurcumin may attenuate the DSS-induced inflammatory response in ulcerative colitis by inhibiting the PI3K/AKT signaling pathway.