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目的:研究半边旗(PsL)提取物Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid(5F)诱导的HepG2细胞凋亡及其可能机制。方法:通过MTT法检测细胞活性以研究HepG2细胞经不同浓度(5~80 mg/L)5F处理24 h所导致的5F细胞毒作用。采用Hoechst/PI实验定性分析细胞凋亡。采用Western blotting实验检测经5F处理的HepG2细胞线粒体内Bax水平及分析cyto-c与AIF在胞浆内的水平。结果:通过细胞活性分析证明,5F对HepG2细胞的细胞毒性随着5F浓度的提高而增强。HepG2经5F处理后,可观察到以细胞核凝聚为特征的凋亡细胞。经5F处理的HepG2细胞线粒体内Bax水平提高,胞浆内cyto-c及AIF水平增强。结论:5F介导的细胞凋亡涉及线粒体依赖途径,5F可能对人类癌细胞具有诱导凋亡作用,尤其是肝细胞癌(HCC)细胞。
Objective: To study the apoptosis of HepG2 cells induced by Ens-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) and its possible mechanism. METHODS: Cell viability of HepG2 cells treated with different concentrations (5-80 mg/L) of 5F for 24 h was detected by MTT assay. Hoechst/PI experiments were used to qualitatively analyze apoptosis. Western blotting was used to detect Bax levels in mitochondria of 5F-treated HepG2 cells and to analyze the cytoplasmic levels of cyto-c and AIF. RESULTS: The cell viability analysis demonstrated that the cytotoxicity of 5F on HepG2 cells increased with the increase of 5F concentration. After HepG2 was treated with 5F, apoptotic cells characterized by nuclear condensation were observed. The level of Bax in the mitochondria of HepG2 cells treated with 5F increased, and the cytoplasmic cyto-c and AIF levels increased. CONCLUSION: 5F-mediated apoptosis involves a mitochondrial-dependent pathway and 5F may have an apoptosis-inducing effect on human cancer cells, especially hepatocellular carcinoma (HCC) cells.