中文摘要：

目的观察SP600125对肿瘤坏死因子（TNF-α）诱导肝癌细胞胰岛素抵抗的改善作用。方法用TNF-α（4 ng/mL）刺激人肝癌细胞HepG2,建立胰岛素抵抗细胞模型。蒽酮法检测细胞内糖原合成;Western blot检测JNK和p-JNK的表达。结果 TNF-α刺激HepG2后细胞内糖原合成障碍,产生胰岛素抵抗。SP600125能显著抑制TNF-α对JNK的激活,并促进细胞内糖原合成。结论 SP600125能改善TNF-α诱导的肝癌细胞胰岛素抵抗。

英文摘要：

Objective To investigate the effect of SP600125 on insulin resistance induced by TNF-α.Methods The insulin resistance cell model were induced by TNF-α（4 ng/mL）to stimulate human hepatoma carcinoma cell HepG2.The intracellular glycogen was detected using a glucose oxidase assay kit.The expression of JNK and p-JNK were observed by Western blot.Results Compared with control,TNF-αtreatment decreased the level of intracellular glycogen in HepG2 cells.However,SP600125 treatment reversed the effect of TNF-α.JNK was activated in response to TNF-α and that effect was reversed by SP600125.Conclusion SP600125 may improve the insulin resistance condition of HepG2 induced by TNF-α.