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中国临床药理学与治疗学 ›› 2011, Vol. 16 ›› Issue (12): 1357-1360.

• 基础研究 • 上一篇    下一篇

18-α异构体甘草酸对化学损伤人肝细胞的保护作用

张群1, 吴培1, 张建军2   

  1. 1东南大学附属中大医院感染病科,南京 210009,江苏;
    2泸州医学院附属医院感染病科,泸州 646000,四川
  • 收稿日期:2011-08-11 修回日期:2011-11-04 出版日期:2011-12-26 发布日期:2012-01-07
  • 通讯作者: 张建军,通信作者,男,博士,主任医师,教授,硕导,研究方向:感染性疾病分子生物学研究。Tel: 13981271009 E-mail: zhangjianjun2535@163.com
  • 作者简介:张群,女,硕士,主治医师,研究方向:肝病的基础与临床。Tel: 13851539978 E-mail: slim888@163.com

Protective effect of 18-α isomer of glycyrrhizin on human hepatocytes injured by D-galactosamine and carbon tetrachloride

ZHANG Qun1, WU Pei1, ZHANG Jian-jun2   

  1. 1Dept. Infectious Diseases, Zhongda Hospital of Southeast University,Nanjing 210009,Jiangsu, China;
    2Dept. Infectious Diseases, Affliated Hospital of Luzhou Medical College, Luzhou 646000,Sichuan, China
  • Received:2011-08-11 Revised:2011-11-04 Online:2011-12-26 Published:2012-01-07

摘要: 目的: 研究18-α异构体甘草酸(异甘草酸镁)对半乳糖胺(D-GalN)和四氯化碳(CCl4)损伤培养人肝细胞(L-02)的保护作用及机制。方法: 培养L-02,用异甘草酸镁进行保护,再经D-GalN或CCl4处理。观察细胞上清活性氮终产物(NOx)含量及细胞线粒体膜电位。结果: 浓度为 1 mg/mL 时, 异甘草酸镁能显著减少D-GaLN和CCl4损伤细胞导致的NOx释放(P<0.05),明显升高D-GaLN损伤所降低的细胞线粒体膜电位。结论: 1 mg/mL 的异甘草酸镁对D-GaLN和CCl4致人肝细胞损伤有明显保护作用,其机制与抑制细胞NOx释放,改善细胞线粒体膜电位作用相关。

关键词: 半乳糖胺, 四氯化碳, 甘草酸, 肝细胞, 药物作用

Abstract: AIM: To investigate the effects of 18-α isomer of glycyrrhizin (magnesium isoglycyrrhizinate,MI) in protecting human hepatocytes (L-02) injured by D-galactosamine (D-GalN) and carbon tetrachloride (CCl4),and research MI in protecting human hepatocytes deeply.METHODS: The cultured L-02 were pre-treated MI,respectively, for protecting these cells from the injury made with CCl4 or D-GalN. Then, the final product of nitrogen (NOx), and the cellular mitochondrial membrane potentials were measured .All the values above were analyzed to research the protective effects of the MI.RESULTS: At the concentration of 1 mg/mL, the MI could improve the survival rate of cells, and significantly reduced NOx releasing from the D-GaLN or CCl4 injured cells(P<0.05), and could increase the decreased cell mitochondrial membrane potential caused by D-GalN.CONCLUSION: At the concentration of 1 mg/mL, the MI have protective effects on the D-GalN or CCl4 injured human hepatocytes. The mechanism of these protective effects may be related to the inhibition of NOx release and related to the improvement of the cellular mitochondrial membrane potentia.

Key words: Galactosamine, Carbon tetrachloride, Glycyrrhizin, Hepatocyte, Drug effects

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