论文部分内容阅读
目的观察白细胞介素37(IL-37)诱导SMMC-7721肝癌细胞凋亡和自噬的机制。方法体外培养SMMC-7721细胞,SMMC-7721细胞分为处理组和对照组,处理组分别予以不同剂量(50、100、200)ng/mL的重组人IL-37(rh IL-37)。CCK-8法检测SMMC-7721细胞增殖能力,流式细胞术检测细胞凋亡,Western blot法检测凋亡和自噬相关蛋白Bax、Bcl-2、微管相关蛋白1轻链3(LC3)和beclin 1及哺乳动物雷帕霉素靶蛋白(mTOR)的水平,透射电子显微镜观察自噬体的形成情况。结果 IL-37可抑制SMMC-7721肝细胞癌细胞的增殖、诱导SMMC-7721细胞凋亡和自噬;IL-37处理组Bax、LC3和beclin 1水平增加,Bcl-2水平降低,mTOR的磷酸化被抑制;可见明显自噬体形成。结论 IL-37可诱导肝细胞癌SMMC-7721细胞发生凋亡和自噬,可能与mTOR的磷酸化有关。
Objective To investigate the mechanism of apoptosis and autophagy induced by interleukin-37 (IL-37) in SMMC-7721 hepatoma cells. Methods SMMC-7721 cells were cultured in vitro. SMMC-7721 cells were divided into treatment group and control group. The treatment groups were given rhIL-37 at different doses (50, 100, 200) ng / mL. The proliferation of SMMC-7721 cells was detected by CCK-8 assay. The apoptosis of SMMC-7721 cells was detected by flow cytometry. The apoptosis and autophagy-related proteins Bax, Bcl-2, LC3 and beclin 1 and mammalian target of rapamycin (mTOR) levels, the formation of autophagosome observed by transmission electron microscopy. Results IL-37 could inhibit the proliferation of SMMC-7721 hepatocellular carcinoma cells and induce the apoptosis and autophagy in SMMC-7721 cells. The levels of Bax, LC3 and beclin 1 were increased and the levels of Bcl-2 were decreased in IL-37 treatment group. Is inhibited; visible autophagosome formation. Conclusion IL-37 can induce apoptosis and autophagy in hepatocellular carcinoma SMMC-7721 cells, which may be related to the phosphorylation of mTOR.