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目的探讨姜黄素在酒精诱导的Hep G2细胞氧化损伤中的保护作用,揭示姜黄素抗酒精性肝损伤的作用机制。方法不同浓度的姜黄素处理Hep G2细胞24 h后,加入酒精诱导细胞损伤。采用MTT检测姜黄素对损伤细胞活力的影响,试剂盒检测细胞中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量以及活性氧(ROS)水平,采用Real-time PCR检测SOD1、SOD2和CAT m RNA的表达。结果 300 mmol/L酒精可致近50%的细胞死亡,4μmol/L的姜黄素对酒精引起的细胞毒性作用保护效果最为显著,可明显改变细胞内SOD活性、MDA含量及ROS水平。与酒精组比较,4μmol/L的姜黄素可显著上调细胞内SOD1、SOD2和CAT m RNA的表达水平。结论姜黄素通过调节细胞的抗氧化能力削弱酒精对肝癌Hep G2细胞的损伤作用。
Objective To investigate the protective effect of curcumin on alcohol-induced oxidative damage in Hep G2 cells and to reveal the mechanism of curcumin on alcohol-induced liver injury. Methods Hep G2 cells were treated with different concentrations of curcumin for 24 h and then induced by alcohol. The effect of curcumin on the viability of damaged cells was detected by MTT assay. The activity of superoxide dismutase (SOD), malondialdehyde (MDA) and reactive oxygen species (ROS) And CAT m RNA expression. Results 300 mmol / L alcohol could cause nearly 50% cell death. Curcumin at 4μmol / L could significantly inhibit the cytotoxicity induced by alcohol and significantly change the intracellular SOD activity, MDA content and ROS level. Compared with alcohol group, 4μmol / L curcumin significantly up-regulated the expression of SOD1, SOD2 and CAT m RNA in cells. Conclusion Curcumin attenuates the injury of Hep G2 cells induced by alcohol by regulating the antioxidant capacity of the cells.