香加皮杠柳苷抑制Stat5信号通路诱导SMMC-7721细胞凋亡的实验研究  

Periplocin of Cortex Periplocae inhibits STAT5 signaling and induces apoptosis in human hepatocellular carcinoma cell line SMMC-7721

作　　者：赵振军[1] 左连富[1] 单保恩[1] 鹿刚 张引娟[1] 张丽杰[2] 

机构地区：[1]河北医科大学第四医院,石家庄050011 [2]河北医科大学第三医院,石家庄050051

出　　处：《临床检验杂志》2008年第1期46-48,共3页Chinese Journal of Clinical Laboratory Science

基　　金：国家自然科学基金项目(No.3037153);河北省自然科学基金项目(No.C2004000610)

摘　　要：目的研究香加皮提取物杠柳苷对Stat5信号通路的影响,探讨其诱导肿瘤细胞凋亡的分子机制。方法MTT比色法检测细胞增殖活性,流式细胞术观察肿瘤细胞的周期变化和凋亡,western blot法检测杠柳苷作用前后人肝癌细胞株SMMC-7721细胞内Stat5蛋白质表达。结果杠柳苷明显抑制SMMC-7721细胞的增殖,使细胞周期停滞在G2/M期,并能够诱导SMMC-7721细胞凋亡。杠柳苷作用后,细胞核内的Stat5蛋白量降低而胞浆中的量未见明显改变。结论香加皮杠柳苷能够抑制Stat5信号转导通路,进而抑制SMMC-7721细胞的增殖并诱导其凋亡。Objective To investigate the effect of Periplocin of Cortex Periplocae （CPP） on STATS signaling and its molecular mechanism of inducing apoptosis and anti-tumor activity. Methods Cell proliferation was studied by MTT assay. Cell apoptosis and cell cycle were investigated by flow cytometry. The effect of CPP on expression of STATS protein in human hepatocellular carcinoma cell line SMMC-7721 ceils was studied by Western blotting. Results CPP inhibited the proliferation significantly and induced apoptosis of SMMC-7721 cells. CPP arrested the cell cycle at G2/M phase. After treated with CPP, the expression level of STATS protein in the cell nucleus decreased but did not significantly changed in cytoplasma. Conclusion CPP inhibits STATS signaling, and then inhibits cell proliferation and induces apoptosis in human hepatocellular carcinoma cellline SMMC-7721.

关 键 词：香加皮杠柳苷 信号传导及转录活化因子 STAT5 流式细胞术 SMMC-7721细胞株 细胞凋亡 

分 类 号：R446.11[医药卫生—诊断学]