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目的:研究药物JKA97对人肝癌细胞HepG2增殖的抑制作用及其分子机制。方法:采用MTT法观察药物JKA97对细胞增殖的影响;倒置显微镜观察细胞形态变化;流式细胞术检测细胞凋亡;Western blot方法检测线粒体融合蛋白mfn2表达水平变化。结果:药物JKA97抑制人肝癌细胞HepG2细胞增殖,5、10、20μmol/L作用组24h抑制率分别为34.26%、43.08%、54.02%;药物JKA97诱导人肝癌细胞HepG2凋亡,10、20μmol/LJKA97作用HepG2细胞24h,细胞凋亡率分别为22.9%、72.9%;线粒体融合蛋白mfn2表达水平显著降低。结论:药物JKA97对人肝癌细胞HepG2生长具有明显的增殖抑制作用,诱导细胞凋亡;线粒体融合蛋白mfn2表达水平降低可能是其重要的分子机制之一。
Objective: To study the inhibitory effect of drug JKA97 on the proliferation of HepG2 human hepatocellular carcinoma cells and its molecular mechanism. Methods: MTT assay was used to observe the effect of JKA97 on cell proliferation. Morphological changes were observed under inverted microscope. Apoptosis was detected by flow cytometry. The expression of mitochondrial fusion protein mfn2 was detected by Western blot. Results: JKA97 inhibited the proliferation of HepG2 cells. The inhibitory rates of JKA97 were 34.26%, 43.08% and 54.02% at 5, 10, and 20μmol / L, respectively. JKA97 induced the apoptosis of HepG2 cells, The apoptosis rate of HepG2 cells was 22.9% and 72.9%, respectively. The mfn2 expression of mitochondrial fusion protein was significantly decreased. Conclusion: The drug JKA97 can significantly inhibit the growth of HepG2 cells and induce apoptosis. The decrease of mfn2 expression may be one of the important molecular mechanisms.