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作 者:刘小美[1] 潘志强[1] 方肇勤[1] 宋菊敏[1] 卢文丽[1] 粱超[1] 张园园[1]
出 处:《上海中医药大学学报》2016年第1期50-54,共5页Academic Journal of Shanghai University of Traditional Chinese Medicine
基 金:国家自然科学基金面上项目(81473562);国家自然科学基金青年基金项目(81503481)
摘 要:目的:观察黄连-大黄-肉桂复方对肝癌细胞增殖的抑制作用,并探索其作用机制。方法:采用醇提法提取黄连-大黄-肉桂复方药液,观察药物作用24 h后SMMC-7721人肝癌细胞株细胞形态的改变;通过MTT法检测不同浓度药物作用24 h、48 h和72 h对肝癌细胞增殖的影响;采用RTq PCR法检测肝癌细胞PTEN、AKT和SGK1基因的mRNA表达。结果:较低浓度的黄连-大黄-肉桂复方作用24 h对肝癌细胞的形态影响较小,而浓度增至2.1 mg/ml可使肝癌细胞部分固缩,大多细胞凋亡,其对肝癌细胞的恶性增殖具有显著抑制作用,并存在时效和量效关系,0.5 mg/ml药物作用48 h即可致肝癌细胞增殖半数得到抑制;药物作用后AKT mRNA表达明显降低,PTEN mRNA表达上调、SGK1 mRNA表达降低。结论:黄连-大黄-肉桂复方能有效抑制肝癌细胞的恶性增殖,且具有时效和量效关系;其抑制作用可能与调节细胞PTEN-PI3K-AKT/SGK1信号转导通路有关。Objective: To observe the inhibiting effect of Rhizoma Coptidis-Rheum Officinale-Cinnamon Compound( RRC) on the proliferation of hepatocellular carcinoma cells and to explore the action mechanism of the compound. Methods:RRC was extracted with alcohol. The morphology of SMMC-7721 cells after 24 hours treatment with RRC was observed and the inhibiting effect on the proliferation of SMMC-7721 cells after 24,48 and 72 hours treatment with different concentration RRC was detected with MTT method. The mRNA expression of PTEN,AKT and SGK1 was measured with RTq PCR method.Results: The hepatocellular carcinoma cells morphology scarcely changed when they were treated with lower concentration RRC,but the cells pyknosis and apoptosis appeared when the concentration of RRC increased to 2. 1mg / ml. RRC could significantly inhibit the malignant proliferation of hepatocellular carcinoma cells. This inhibiting effect existed time-effect and dose-effect relationship. About half hepatocellular carcinoma cells were inhibited when they treated with 0. 5mg / ml RRC for 48 hours. Meanwhile,RRC down-regulated AKT( P〈0. 05) and SGK1 mRNA expression and up-regulated PTEN mRNA expression of hepatocellular carcinoma cells. Conclusion: RRC can effectively inhibit the proliferation of hepatocellular carcinoma cells and the inhibition appears time-effect and dose-effect relationship. The effect of RRC may has the relationship with regulating the PTEN-PI3K-AKT / SGK1 pathway.
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