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研究了灵芝肽(GLP)在体外对人肝癌HepG2细胞凋亡的影响,并初步探讨了其作用机制。结果显示,透射电镜下可见细胞染色质浓缩、聚集于核边缘成块状,形成典型的凋亡小体;GLP使HepG2细胞阻滞于G0/G1期,随着GLP浓度升高,其G0/G1期的细胞比例随之增加;同时细胞的早期、晚期和总的凋亡率亦均随之增加,存在剂量-效应关系;Western blotting检测结果显示,抑制凋亡基因bcl-2和survivin表达下调,而促凋亡基因p53表达上调,并且都存在剂量依赖性;细胞凋亡的关键蛋白酶caspase-3被激活,并且caspase-3酶活性与GLP浓度亦有剂量依赖性。提示GLP体外可诱导人肝癌HepG2细胞凋亡,其作用机制可能与bcl-2和survivin表达下调、p53表达上调及Caspase-3被激活有关。
The effects of Ganoderma lucidum peptides (GLP) on the apoptosis of human hepatocellular carcinoma HepG2 cells were studied in vitro and its mechanism was also discussed. The results showed that under the transmission electron microscopy, the chromatin of the cells concentrated and aggregated to the edge of nucleus to form a typical apoptotic body. GLP blocked HepG2 cells in G0 / G1 phase. With the increase of GLP concentration, the G0 / The proportion of cells in G1 phase increased with the increase of cell cycle. The early, late and total cell apoptosis rate also increased with the dose-effect relationship. The results of Western blotting showed that the expression of apoptosis-inhibiting genes bcl-2 and survivin were down-regulated , And the expression of pro-apoptotic gene p53 was up-regulated, and both in a dose-dependent manner. Caspase-3, a key protease involved in apoptosis, was activated, and caspase-3 activity was also dose- These results suggest that GLP can induce apoptosis of human HepG2 cells in vitro. The mechanism may be related to down-regulation of bcl-2 and survivin, up-regulation of p53 and activation of Caspase-3.