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机构地区:[1]东南大学附属中大医院感染病科 [2]泸州医学院附属医院感染病科
出 处:《中国临床药理学与治疗学》2011年第12期1357-1360,共4页Chinese Journal of Clinical Pharmacology and Therapeutics
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1mg/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:1mg/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。To investigate the effects of 18-α isomer of glycyrrhizin (magnesium isoglycyrrhizinate, MI) in protecting human hepatocytes (L-02) injured by D galactosamine (DGalN) and carbon tetrachloride (CCL),and research MI in protecting human hepatocytes deeply. METHODS: The cultured L-02 were pretreated MI, respectively, for protecting these ceils from the injury made with CC14 or DGaIN. 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 rag/ mL, the MI could improve the survival rate of cells, and significantly reduced NO_x releasing from the DGaLN or CC14 injured cells (p 0.05), and could increase the decreased cell mi- tochondrial membrane potential caused by DGAIN. CONCLUSION: At the concentration of 1 mg/mL, the MI have protective effects on the DGalN or CC. injured human hepatocytes. The mechanism of these protective effects may be re- lated to the inhibition of NOx release and related to the improvement of the cellular mitochondrial membrane potentia.
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