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作 者:张丽杰[1] 鹿刚 张引娟[2] 刘刚叁[3] 单保恩[2]
机构地区:[1]河北医科大学第三医院检验科,石家庄050051 [2]河北医科大学第四医院科研中心,石家庄050011 [3]华北制药集团新药研究开发有限责任公司,石家庄050015
出 处:《第三军医大学学报》2008年第15期1448-1451,共4页Journal of Third Military Medical University
基 金:国家自然科学基金(3037153);河北省自然科学基金(C2004000610)~~
摘 要:目的研究香加皮提取物杠柳苷对Stat3信号通路的影响,及其诱导细胞凋亡的分子机制。方法MTT比色法检测人肝癌细胞SMMC-7721增殖活性,流式细胞术分析肿瘤细胞的周期变化和凋亡,Western blot检测细胞内Stat3蛋白表达,RT-PCR检测细胞Mcl-1、Survivin和XIAP mRNA的表达。结果杠柳苷可明显抑制SMMC-7721细胞的增殖,诱导SMMC-7721细胞凋亡,并使细胞周期停滞在G2/M期。杠柳苷作用后,细胞核内Stat3量降低,而细胞质中的量未见明显改变,细胞内Mcl-1、Survivin和XIAP基因的表达明显降低,并呈时间依赖性。结论香加皮提取物杠柳苷通过抑制Stat3信号转导通路和Mcl-1、Survivin和XIAP mRNA的表达,进而抑制SMMC-7721细胞的增殖,诱导其凋亡。Objective To investigate the effect of periplocin of cortex periplocae (CPP) on Star3 signaling and its probable molecular mechanism of inducing apoptosis and anti-tumor activity. Methods Cell proliferation was detected by MTT. Cell apoptosis and cell cycle were investigated by flow cytometry. Expression of Star3 protein in SMMC-7721 cells was analyzed by Western blot. Mcl-1, Survivin and XIAP mRNA expressions were measured by RT-PCR. Results CPP inhibited the proliferation of SMMC-7721 cells significantly, induced their apoptosis and arrested their cell cycle at G2/M phase. Decreased expression of Stat3 protein in the cell nucleus was observed after CPP treatment, but no significant changes were found in cytoplasma. Mcl-1, Survivin and XIAP mRNA expression levels were decreased in a time-dependent manner. Conclusion CPP inhibits cell proliferation and induces apoptosis by inhibiting Stat3 signal transduction in human hepatocellular carcinoma cell line SMMC-7721.
关 键 词:香加皮杠柳苷 信号转导 转录活化因子 Star3 Western blot 流式细胞术 SMMC-7721细胞株
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