中文摘要：

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。

英文摘要：

Objective：To investigate the inhibitory effect of JKA97 on proliferation and the molecular mechanism of human liver cancer cell line HepG2 in vitro.Methods：The cell viability was detected by MTT[3-（4,5-Dimethylthiazol-2-yl）-2,5-diphenyl tetrasoliumBromide];Morphological changes of HepG2 cells were measured by microscope;JKA97 induced apoptosis of HepG2 cells was detected by AnnexinV-PI staining and flow cytometry;The expression of mitochondria-shaping protein,mitofusin-2（mfn2）was measured by Western blot.Results：JKA97 induced the apoptosis of HepG2 cells and the expression level of mfn2 decreaed gradually. Conclusion：JKA97 can obviously inhibit the proliferation of human liver cancer cell line HepG2 in vitro and induce apoptosis of HepG2 cells.Lower expression of mitochondrial fusion protein mfn2 may be one of JKA97＇s molecular mechanisms.