| 李兰芳，郭玉，唐国涛，喻翠云，陈临溪.SP600125改善TNF-α诱导的肝癌细胞胰岛素抵抗.[J].中南医学科学杂志.,2011,39(2):160-161. |
| SP600125改善TNF-α诱导的肝癌细胞胰岛素抵抗 |
| SP600125 Improve the Insulin Resistance of HepG2 Induced by TNF-α |
| 投稿时间：2010-09-02 |
| DOI： |
| 中文关键词: 胰岛素抵抗 肿瘤坏死因子α 肝癌细胞 |
| 英文关键词:insulin resistance TNF-α hepatoma carcinoma cells |
| 基金项目:国家自然科学基金(30901577)、湖南省衡阳市科技局项目资助(2009KJ14). |
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| 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: |
| ObjectiveTo investigate the effect of SP600125 on insulin resistance induced by TNF-α.MethodsThe 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.ResultsCompared 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.ConclusionSP600125 may improve the insulin resistance condition of HepG2 induced by TNF-α. |
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