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中国临床药理学与治疗学 ›› 2010, Vol. 15 ›› Issue (2): 140-144.

• 基础研究 • 上一篇    下一篇

吡格列酮降低胰岛素抵抗状态下的氧化应激水平

李兰芳, 郭玉, 唐国涛, 陈淑娴, 陈临溪   

  1. 南华大学药物药理研究所,衡阳 421001,湖南
  • 收稿日期:2009-10-29 修回日期:2009-12-14 出版日期:2010-02-26 发布日期:2020-09-18
  • 通讯作者: 陈临溪,男,教授,主要研究方向:心血管药理与药物蛋白质组学。Tel: 0734-8281408 E-mail: chenlinxi@tom.com
  • 作者简介:李兰芳,女,硕士,研究方向:2型糖尿病的分子机制研究。Tel: 13264130629 E-mail: wjliu829@yahoo.cn
  • 基金资助:
    国家自然科学基金资助(30901577);湖南省衡阳市科技局项目(2009KJ14)资助

Pioglitazone decrease the level of oxidative stress of insulin resistance

LI Lan-fang, GUO Yu, TANG Guo-tao, CHEN Shu-xian, CHEN Lin-xi   

  1. Institute of Pharmacy and Pharmacology, Nanhua University,Hengyang 421001, Hunan, China
  • Received:2009-10-29 Revised:2009-12-14 Online:2010-02-26 Published:2020-09-18

摘要: 目的:探讨吡格列酮对胰岛素抵抗状态下的氧化应激水平的影响。 方法:分别用TNF-α(4 ng/mL)和高浓度胰岛素(10-7 mol/L)刺激人肝癌细胞HepG2,建立胰岛素抵抗细胞模型。MTT法观察细胞毒性作用;氧化酶法检测细胞培养液中的葡萄糖浓度;用DCF-DA探针标记,流式细胞仪检测细胞内活性氧的水平;免疫荧光检测NF-κB核转位。 结果:TNF-α和高浓度胰岛素刺激HepG2后,导致葡萄糖摄取障碍,细胞培养液上清中葡萄糖浓度较对照组显著升高,同时细胞内活性氧的水平较对照组也显著升高。吡格列酮显著改善胰岛素抵抗状态,同时显著降低细胞内氧化应激的水平。吡格列酮还能逆转TNF-α和高浓度胰岛素引起的NF-κB核转位。结论:吡格列酮能抑制NF-κB核转位,降低氧化应激水平,改善胰岛素抵抗状态。

关键词: 胰岛素抵抗, 氧化应激, TNF-α, NF-κB

Abstract: AIM: To investigate the effects of pioglitazone on oxidative stress and insulin resistance. METHODS: The insulin resistance cell model was induced by TNF-α(4 ng/mL)and high dose of insulin(10-7 mol/L) to stimulate human hepatoma carcinoma cell HepG2. The cytotoxicity of HepG2 was observed by MTT. The concentration of glucose in cell culture fluid of HepG2 was detected using a glucose oxidase assay kit. The level of intracellular reactive oxygen species (ROS) was detected by DCFH-DA fluorescent probe and flow cytometry. The translocation of NF-κB was observed by immunofluorescence. RESULTS: Compared with control, TNF-αand high dose of insulin treatment significantly increased the level of ROS in HepG2 and the concentration of glucose in the cultrure medium of HepG2. However, pioglitazone treatment could reverse those effects of TNF-α and high dose of insulin. NF-κB translocated to nuclear stimulated by TNF-αand high dose of insulin. Pioglitazone could inhibit the translocation of NF-κB. CONCLUSION: Pioglitazone improve the insulin resistance condition by degrading oxidative stress level and inhibiting the translocation of NF-κB.

Key words: Insulin resistance, Oxidative stress, TNF-α, NF-κB

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