促炎细胞因子
炎症
炎症性肠病
结肠炎
脂多糖
化学
免疫学
药理学
医学
内科学
疾病
作者
Haihua Zhang,Haijun Gu,Qinghui Jia,Yanqing Zhao,Hongqiang Li,Shurui Shen,Xin Liu,Guisheng Wang,Shi QiuMei
标识
DOI:10.1016/j.abb.2019.108242
摘要
Inflammatory bowel disease (IBD) is a chronic inflammatory condition with high incidence. Syringin exhibits multiple pharmacological properties, including anti-inflammatory effects. However, the effect of syringin on inflammation of IBD is still unclear. Here, the dextran sulfate sodium (DSS)-induced colitis model was established in vivo. Rat intestinal epithelium IEC6 cells were treated with lipopolysaccharide (LPS) in vitro. Syringin inhibited DSS or LPS-induced overproduction of proinflammatory cytokines (IL-1β, IL-6, TNF-α) and proinflammatory substances (iNOS, COX-2). Moreover, syringin inactivated the proinflammatory NF-κB p65 pathway by decreasing IκBα phosphorylation at Ser 32. The activation of antioxidant Nrf2 signaling pathway was promoted by syringin. Additionally, LPS-induced inflammation in IEC6 cells was also suppressed by NF-κB inhibitor PDTC and Nrf2 activator RTA408. The anti-inflammatory effects of syringin were comparable to these two reagents. Taken together, our results suggest that syringin shows protective effects on intestinal inflammation through inhibiting NF-κB, while activating Nrf2 signaling pathway in colitis.
科研通智能强力驱动
Strongly Powered by AbleSci AI