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作 者:赵晓艳[1] 胡玉娜[1] 康向东[1] 张隆[1] 季青[1] 倪振华[1]
机构地区:[1]上海中医药大学附属普陀医院中心实验室,上海200062
出 处:《中国癌症杂志》2010年第2期101-104,共4页China Oncology
摘 要:背景与目的:熊果酸(ursolic acid,UA)广泛存在于夏枯草、白花蛇舌草等清热解毒药中,可抑制多种肿瘤细胞增殖并诱导其凋亡,具有广泛生物学活性。本研究将UA作用于人胃癌BGC823细胞,观察其对细胞凋亡的影响,并探讨其可能的作用机制。方法:MTT法检测UA对BGC823细胞增殖的影响;流式细胞术检测细胞周期与凋亡的变化;Realtime-PCR检测细胞bax、bcl-2mRNA表达的变化。结果:UA呈时间-剂量依赖性抑制BGC823细胞增殖,分别作用24、48、72h后半数抑制浓度依次为36.88、34.72、32.18μmol/L;UA能诱导BGC823细胞凋亡,并阻滞细胞于G2/M期;此外,其还可上调BGC823细胞bax及下调bc1-2mRNA表达,且作用随剂量的增加而加强。结论:UA呈时间-剂量依赖性抑制BGC823细胞增殖,并诱导其凋亡,阻滞细胞于G2/M期;其凋亡机制可能与上调bax及下调bcl-2基因的表达有关。Background and purpose:Ursolic acid is widely present in spica prunellae, hedyotis diffusa and other heat antidotes. The growth of a variety of tumor cells can be inhibited and induced apoptosis by ursolic acid. This study was aimed to investigate the effect and possible mechanisms of UA on inducing apoptosis of human gastric carcinoma BGC823 cells. Methods:The MTT assay was used to detect the antiproliferative effect of UA on BGC823 cells. Flow cytometry was used to detect cell cycle and apoptosis of BGC823 cells. The expression level of bcl-2 and bax gene was investigated by real time-polymerase chain reaction (real time-PCR). Results:UA inhibited the proliferation of BGC823 cells in a dose and time-dependent way. After treatment by UA for 24, 48 and 72 h, the IC50 of BGC823 was 36.88, 34.72, and 32.18 μmol/L, respectively. UA could significantly induce apoptosis of BGC823 cells and block cells at G2/M phase. UA could increase the expression of bax gene and decrease the expression of bcl-2 gene in a dose and time-dependent way. Conclusion:UA could induce apoptosis and inhibit the proliferation of B?C823 cells in a dose and time-dependent way. It could arrest cell cycle of BGC823 cells at G2/M phase. Its mechanisms might be associated with the up-regulation of bax gene and down-regulation of bcl-2 gene.
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