白藜芦醇通过PI3K/AKT信号通路抑制脂多糖诱导的人牙龈成纤维细胞炎症

Resveratrol inhibits human gingival fibroblast inflammation induced by lipopolysaccharide through PI3K/AKT signaling pathway

目的:探讨白藜芦醇(RSV)对牙龈卟啉单胞菌脂多糖(LPS)诱导的人牙龈成纤维细胞(HGFs)炎症的调控及其与PI3K/AKT信号通路的相关性。方法:空白对照组、RSV组、LPS组、LPS+RSV组,通过CCK-8法评估细胞活力。然后,设置空白对照组、LPS组、LPS+RSV组,通过酶联免疫吸附(ELISA)测定炎症因子白细胞介素-1β(IL-1β)、IL-6、IL-8和肿瘤坏死因子-α(TNF-α)的水平;通过Western blot分析PI3K/AKT信号通路相关蛋白的表达水平。最后,设置空白对照组、LPS组、LPS+RSV组、LPS+RSV+LY294002组,ELISA测定炎症因子水平;通过Western blot分析PI3K/AKT信号通路的激活情况。结果:RSV对HGFs无细胞毒性;在LPS诱导的HGFs炎症中,RSV下调IL-1β、IL-6、IL-8和TNF-α水平;RSV可诱导PI3K/AKT信号通路失活;且PI3K/AKT信号通路抑制剂(LY294002)能通过下调IL-1β、IL-6、IL-8和TNF-α表达,进一步增强RSV的抗炎效果。结论:RSV可通过抑制PI3K/AKT信号通路,减轻LPS诱导的HGFs的炎症反应。

Objective:To investigate the regulatory mechanism of Resveratrol(RSV) on Lipopolysaccharide(LPS)-induced inflammation of human gingival fibroblasts(HGFs) and its correlation with PI3 K/AKT signaling pathway.Methods: Blank control group, RSV group, LPS group and LPS+RSV group were set up to evaluate cell viability by CCK-8 method.The blank control group, LPS group and LPS+RSV group were set up to determine the levels of inflammatory cytokines IL-1β,IL-6,IL-8 and TNF-α by ELISA and analyze the expression levels of PI3 K/AKT signaling pathway related proteins by Western blot.The blank control group, LPS group, LPS+RSV group, LPS+RSV+LY294002 group were set up to determine the levels of inflammatory cytokines IL-1β,IL-6,IL-8 and TNF-α by ELISA and analyze the activation of PI3 K/AKT signaling pathway by Western blot.Results:RSV was not toxic to HGFs.RSV down-regulated the levels of IL-1β,IL-6,IL-8 and TNF-α in LPS induced HGFs inflammation.RSV induced inactivation of the PI3 K/AKT signaling pathway.PI3 K/AKT pathway inhibitor(LY294002) could further enhance the anti-inflammatory effect of RSV by down-regulating the expression of IL-1β,IL-6,IL-8 and TNF-α.Conclusion:RSV can reduce Lps-induced inflammation of HGFs by inactivating PI3 K/AKT signaling pathway.