中文摘要：

目的：探讨姜黄素对游离脂肪酸（FFA）诱导HepG2细胞造成的非酒精性脂肪性肝炎（NASH）细胞模型胰岛素抵抗及炎症的影响。方法：用500μmol/L的FFA诱导HepG2细胞24h,建立NASH体外模型;用不同浓度的姜黄素干预NASH体外模型,MTT法检测姜黄素的安全药物浓度范围;油红O染色观察细胞内脂肪变;Elisa法检测细胞培养上清液中白介素（IL-8）、肿瘤坏死因子-α（TNF-α）及葡萄糖转运蛋白-4（GLUT4）;Western-blot法测定细胞胰岛素受体（IR）的蛋白表达。结果：①NASH细胞模型组培养液中IL-8、TNF-α含量明显高于空白对照组,GLUT4含量明显低于空白对照组,IR蛋白表达明显低于空白对照组（P〈0.01）;②NASH模型组中同时加入姜黄素可明显改善细胞脂肪样变,减少炎性因子分泌（P〈0.01,P〈0.05）,提高IR蛋白表达及GLUT4含量（P〈0.01）。结论：姜黄素能够通过影响IR、GLUT4、IL-8、TNF-α改善NASH体外模型的胰岛素抵抗及炎症反应。

英文摘要：

Objective： To investigate the effects of curcumin on anti inflammatory and anti insulin resistant in nonalcoholic steatohepatitis （NASH） cell model. Methods： To establish a NASH cell model by inducing HepG2 cells with 500tnnol/L FFA for 24 hours. For the intervention, different concentrations of curcumin were prepared. Cell viability was detected by MTF to explore the safe range of concentrations; intracellular lipid droplets were detected by oil red O staining; IL-8, TNF-a and GLUT4 in supernatant were tested by Elisa. Western blot method was used to detect Insulin Receptor （IR） protein expression. Results： After FFA induced for 24 hours, oil red staining showed steatosis; IL-8 and TNF-a in supernatant in model group were significantly higher than the control group （P〈0.01）, while the contents of GLUT4 and IR expression were less than the control group （P〈0.01）. With the intervention of curcumin, the intracellular lipid droplets changed, the secretion of inflammatory factors decreased （P〈0.01, P〈0.05）, the protein expression of IR and GLUT4 enhanced （P〈0.01）. Conclusion： Curcumin exhibits an anti insulin resistant and anti inflammatory effects in NASH cell model.