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目的:观察异常黑胆质成熟剂乙酸乙酯萃取物(ASMq-EtOAc)对人肝癌细胞株(HepG2)生长和凋亡及相关基因调控的作用,探讨其抗癌的物质基础和作用机理。方法:采用四氮甲基唑蓝法(MTT)观察了ASMq-EtOAc对HepG2细胞体外生长的抑制作用;采用琼脂糖凝胶电泳技术和流式细胞术观察ASMq-EtOAc对HepG2细胞凋亡的影响;采用逆转录-多聚酶链式反应技术(RT-PCR)观察ASMq-EtOAc对HepG2细胞凋亡相关基因mRNA表达的影响。结果:ASMq-EtOAc明显抑制HepG2细胞体外生长、诱导细胞凋亡、阻滞细胞周期、明显提高抑癌基因p53、p21基因mRNA的表达,对Bcl-2、Bax基因mR-NA表达不产生明显的影响。结论:ASMq-EtOAc可能是异常黑胆质成熟剂抗癌作用的主要活性部位之一,其抗癌作用可能通过诱导癌细胞凋亡、改变癌细胞周期和促进抑癌基因p53及p21表达来实现。
OBJECTIVE: To observe the effect of ASMq-EtOAc on the growth and apoptosis of HepG2 cells and the regulation of related genes, and to explore the material basis and mechanism of anticancer activity. Methods: The inhibitory effect of ASMq-EtOAc on the growth of HepG2 cells was observed by MTT assay. The effect of ASMq-EtOAc on the apoptosis of HepG2 cells was observed by agarose gel electrophoresis and flow cytometry The effect of ASMq-EtOAc on the mRNA expression of apoptosis-related genes in HepG2 cells was observed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: ASMq-EtOAc significantly inhibited the growth of HepG2 cells in vitro, induced apoptosis, blocked the cell cycle and significantly increased the mRNA expression of tumor suppressor genes p53 and p21, but did not significantly affect the expression of mR-NA of Bcl-2 and Bax influences. CONCLUSION: ASMq-EtOAc may be one of the major active sites of anticancer effect of abnormal savda. Its anticancer effect may be achieved by inducing apoptosis of cancer cells, changing the cell cycle of cancer and promoting the expression of tumor suppressor genes p53 and p21 .