温郁金二萜类化合物C对脂多糖诱导的人胃腺癌SGC7901细胞内NF-κB信号通路的影响

摘要

AIM; To observe lhe effecls of dilerpenoid C from elher exlracL of Radix Curcumae (RC) on lhe ac-Livily of nuclear faclor - kB in human gaslric adenocarcinoma SGC7901 cells slimulaled wilh lipopolysaccharide (LPS). METHODS; SGC7901 cells were normally cultured, induced by LPS, or Irealed wilh LPS plus RC. The prolein expression of IKKct, IKK(3, p65, phosphorylaled p65 and phosphorylaled IkBa was assayed by Weslern blolling. NF - kB DNA binding aclivily was determined by eleclrophorelic mobilily shifl assay. RESULTS: RC reduced lhe prolein expression of IKKct, IKKβ, p65, phosphorylaled p65 and phosphorylaled IkBo: induced by LPS. NF - kB DNA binding aclivily increased much greally by LPS stimulation, while RC resisted lhe action of LPS. CONCLUSION; RC may allenuale lhe se-crelion of inflammatory cylokines by inhibiting lhe activation of NF - kB signaling pathway.%目的:研究温郁金二萜类化合物C(RC)对脂多糖诱导的人胃腺癌SGC7901细胞核因子-κB(nuclear factor kappa B,NF-κB)活性影响.方法:以10 mg/L脂多糖(LPS)刺激体外培养的SGC7901细胞建立炎症模型,设正常对照组、LPS刺激组、RC预干预组(RC干预后以LPS刺激).蛋白质印迹法检测IKK、p-p65、p65和p-IκBα蛋白表达,凝胶迁移阻滞实验检测p65与DNA结合活性.结果:与炎症模型组比较,经温郁金二萜类化合物干预后,细胞中的IKK、p-p65、p65和p-IκBα蛋白表达均减少;入核p65蛋白与DNA结合活性减弱.结论:温郁金二萜类化合物通过抑制核因子-κB信号通路起抗炎作用.