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以H2O2建立Chang liver细胞损伤模型,设空白对照组、损伤模型组、黄芪甲苷保护组、毛蕊异黄酮葡糖苷保护组、芒柄花素保护组和阳性对照组。采用四甲基偶氮唑盐(MTT)法、微板法、流式细胞术、DNA Ladder检测等方法测定细胞存活率、细胞外液转氨酶活性、周期分布及凋亡情况。结果显示H2O2的诱导使Chang liver细胞存活率降低、活性升高、发生G0/G1期阻滞及细胞外液转氨酶、细胞凋亡率的升高,3种成分对细胞的预处理均可显著或极显著的升高细胞存活率、缓解G0/G1期的阻滞现象、并降低细胞外液转氨酶活性及细胞凋亡率(P<0.05或P<0.01)。表明黄芪主要成分(黄芪甲苷、毛蕊异黄酮葡糖苷和芒柄花素)对H2O2诱导的Chang liver细胞凋亡均有一定的抑制作用。
The model of Chang liver cell injury was established by H2O2. The blank control group, injury model group, astragaloside protection group, calycosin protection group, and metformin protection group and positive control group were established. Cell survival rate, transaminase activity, cycle distribution and apoptosis were measured by MTT assay, microplate assay, flow cytometry and DNA Ladder assay. The results showed that the induction of H2O2 decreased the cell viability, increased the activity of G0 / G1 phase, and increased the transaminase and apoptosis rate in the extracellular fluid. The pretreatments of the three components were significant or Significantly increased the cell viability, alleviated the arrest in G0 / G1 phase and decreased the transaminase activity and apoptosis rate in extracellular fluid (P <0.05 or P <0.01). The results showed that the main constituents of astragalus (Astragaloside IV, calycosin and formononetin) had a certain inhibitory effect on H2O2-induced apoptosis of Chang liver cells.