论文部分内容阅读
目的观察姜黄素对人肝癌细胞株HepG2体外增殖和端粒酶活性的影响,为彰明其抗肝癌机制提供依据。方法四甲基偶氮唑蓝(MTT)实验检测细胞生长抑制率;流式细胞法检测细胞周期的分布;端粒片断重复扩增-酶联免疫吸附法(TRAP-ELISA)测定细胞端粒活性的变化;并用RT-PCR法检测细胞端粒酶hTERT-mRNA的表达。结果姜黄素对HepG2细胞生长有显著的抑制作用,并呈明显的量效依赖性;不同浓度的姜黄素使G2/M期细胞比例明显增加,G1期/细胞比例明显降低;随姜黄素浓度的增加,HepG2细胞端粒酶活性依次下降;不同浓度提取物对HepG2细胞的hTERT-mRNA表达均有明显抑制作用,具有显著的量效关系。结论姜黄素对HepG2细胞有明显的生长抑制作用,可能作用机制为诱导细胞周期G2/M期阻滞并抑制HepG2细胞端粒酶hTERT-mRNA的转录,从而降低端粒酶的活性。
Objective To observe the effects of curcumin on the proliferation and telomerase activity of human hepatocellular carcinoma cell line HepG2 in order to provide evidence for its mechanism of anti-liver cancer. Methods MTT assay was used to detect cell growth inhibition rate. Cell cycle distribution was analyzed by flow cytometry. Telomeric repeat amplification-enzyme-linked immunosorbent assay (TRAP-ELISA) The changes of telomerase hTERT-mRNA expression were detected by RT-PCR. Results Curcumin significantly inhibited the growth of HepG2 cells and showed a dose-dependent manner. Curcumin at different concentrations significantly increased the percentage of cells at G2 / M phase and decreased the percentage of cells at G1 / Increased, the telomerase activity of HepG2 cells decreased in turn; different concentrations of extract on HepG2 cells hTERT-mRNA expression were significantly inhibited, with a significant dose-effect relationship. Conclusion Curcumin can significantly inhibit the growth of HepG2 cells. The possible mechanism is that it inhibits the cell cycle G2 / M arrest and inhibits the transcription of telomerase hTERT-mRNA in HepG2 cells, thus decreasing the activity of telomerase.