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目的:探讨黄芪甲苷对Chang Liver细胞酒精性和非酒精性氧化损伤的保护作用。方法:以Chang Liver细胞为研究对象,使用乙醇、H2O2分别建立酒精性及非酒精性氧化损伤模型,MTT法测定细胞存活率,微板法、比色法检测转氨酶活力及抗氧化能力,DCF荧光法检测细胞内活性氧,流式细胞术检测细胞周期,DNA ladder法检测细胞凋亡。结果:2种氧化损伤均可导致Chang Liver细胞存活率和抗氧化酶活性下降、以及细胞外液中转氨酶活力和丙二醛含量升高,黄芪甲苷对上述损伤均有显著或极显著的保护效果;同时,乙醇能够显著降低损伤细胞内的活性氧水平,而H2O2能够显著升高损伤细胞内的活性氧水平,黄芪甲苷则能使上述异常的活性氧水平趋于正常。同时缓解乙醇或H2O2对Chang Liver细胞G0/G1期的阻滞现象,并对二者诱导的细胞凋亡均有一定的抑制作用。结论:黄芪甲苷对Chang Liver细胞的酒精性和非酒精性氧化损伤均有保护作用。
Objective: To investigate the protective effects of Astragaloside on alcoholic and non-alcoholic oxidative damage in Chang liver cells. Methods: The model of Chang Liver cells was established. Ethanol and H2O2 were used to establish alcoholic and non-alcoholic model of oxidative injury. MTT assay was used to determine the cell viability. The cell viability was measured by microplate assay. The activity of aminotransferase and antioxidant activity were measured by colorimetry. DCF fluorescence The intracellular reactive oxygen species (ROS) were detected by flow cytometry. The cell cycle was detected by flow cytometry. Apoptosis was detected by DNA ladder. Results: Both oxidative damage led to the decrease of cell viability and antioxidant enzyme activity of Chang liver cells and the increase of aminotransferase and malondialdehyde content in extracellular fluid. Astragaloside had significant or extremely significant protection against these injuries At the same time, ethanol can significantly reduce the level of reactive oxygen species in injured cells, and H2O2 can significantly increase the level of reactive oxygen species in injured cells, Astragaloside A can make the abnormal level of reactive oxygen species to normal. At the same time, it can alleviate the block of G0 / G1 phase of Chang Liver cells induced by ethanol or H2O2 and inhibit the apoptosis induced by both of them. Conclusion: Astragaloside has a protective effect on alcoholic and non-alcoholic oxidative damage of Chang liver cells.