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目的探讨人参皂苷Rg1(Ginsenoside Rg1,Rg1)对白消胺(Busulfan,BU)诱导的人胚肺成纤维细胞衰老的延缓作用。方法将人胚肺成纤维细胞(<24代)随机分为空白对照组(常规培养)、BU组(以120μmol/L BU处理复制细胞衰老模型)、BU+Rg1组(120μmol/L BU+10μmol/L Rg1)、Rg1预+BU组(10μmol/L Rg1预处理后加入120μmol/L BU)和Rg1预+BU+Rg1组(10μmol/L Rg1预处理后加入120μmol/L BU,再加入10μmol/L Rg1),通过倒置显微镜观察细胞形态的变化,细胞增殖试验检测细胞增殖情况,流式细胞术分析细胞周期的分布;半乳糖苷酶(SA-β-gal)染色法观察细胞衰老情况。结果 BU组细胞胞体扁平、宽大、不规则,出现空泡,而Rg1处理各组细胞的衰老表型出现一定程度的改善,以Rg1预+BU+Rg1组效果最佳,但未完全恢复;BU组细胞增殖能力较空白对照组明显降低,Rg1处理组细胞增殖能力有所恢复,且随着时间的延长效果越明显,其中以Rg1预+BU+Rg1组最佳;Rg1预+BU组和Rg1预+BU+Rg1组G2/M期比例较BU组显著降低(P<0.05),其中以Rg1预+BU+Rg1组降低最明显;Rg1预+BU组和Rg1预+BU+Rg1组衰老细胞数较BU组显著降低(P<0.05)。结论 Rg1能有效对抗BU诱导的细胞早衰,其具体作用机制有待进一步深入研究。
Objective To investigate the delayed effect of Ginsenoside Rg1 (Rg1) on the senescence of human embryonic lung fibroblasts induced by Busulfan (BU). Methods Human embryonic lung fibroblasts (<24 passages) were randomly divided into blank control group (conventional culture), BU group (replicated cell senescence model treated with 120μmol / L BU), BU + Rg1 group (120μmol / L BU + / L Rg1 pretreatment + BU group (120μmol / L BU after 10μmol / L Rg1 preconditioning) and Rg1 + BU + Rg1 pretreatment (10μmol / L Rg1 pretreatment by 120μmol / L BU) L Rg1). The morphological changes of the cells were observed by inverted microscope. Cell proliferation was detected by cell proliferation assay. Cell cycle distribution was analyzed by flow cytometry. Cell senescence was observed by the method of SA-β-gal staining. Results The cell bodies of BU cells were flat, wide, irregular and vacuolated. However, the aging phenotype of cells treated with Rg1 was improved to a certain degree, and the best results were obtained with Rg1 + BU + Rg1 group, but not fully recovered. Rg1 pretreatment + BU group and Rg1 pre + BU group and Rg1 + BU + Rg1 + Rg1 + BU group were the best, The proportion of G2 / M phase in pre + BU + Rg1 group was significantly lower than that in BU group (P <0.05), and the most obvious decrease was in Rg1 pre + BU + Rg1 group; the senescent cells in Rg1 pre + BU group and Rg1 pre + BU + Rg1 group The number was significantly lower than BU group (P <0.05). Conclusion Rg1 can effectively antagonize BU-induced premature senility and its specific mechanism of action needs further study.