[丹参酮ⅱA诱导鼻咽癌细胞株凋亡及其分子机制研究]。

Shulan Yuan, Yanping Wang, Xiaohe Chen, Yi Song, Yan Yang
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引用次数: 0

摘要

目的:观察丹参酮ⅱA对人鼻咽癌(NPC)细胞株CNE-1凋亡的影响并探讨其作用机制。方法:用0.5微克/毫升丹参酮II A处理体外培养的CNE-1细胞4 d。显微镜下观察细胞形态。通过细胞计数测定细胞的生长和增殖情况。凝胶电泳检测DNA断裂。流式细胞术检测细胞周期、凋亡指数(AI)及凋亡相关基因的表达。结果:0.5微克/毫升丹参酮ⅱA可诱导CNE-1细胞凋亡。治疗组观察到凋亡细胞的形态学特征,细胞DNA呈“阶梯”状断裂,细胞生长和增殖受到明显抑制,AI为16.9%(对照组为6.4%)。细胞停留在G0/G1期,细胞DNA合成受到抑制。凋亡相关基因fas、bax、p53、p21表达上调;bcl-2表达下调。结论:丹参酮ⅱA可诱导人鼻咽癌细胞凋亡。其分子机制可能与调控细胞凋亡相关基因的表达有关。
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[A study on apoptosis of nasopharyngeal carcinoma cell line induced by Tanshinone II A and its molecular mechanism].

Objective: To assess effect of Tanshinone II A on the apoptosis of human nasopharyngeal carcinoma (NPC) cell line CNE-1 and inquire into the mechanism there in involved.

Methods: The CNE-1 cells cultured in vitro were treated with 0.5 microgram/ml Tanshinone II A for 4 days. The morphology of the cells was observed by microscopy. The cell growth and proliferation were measured by cell counting. The DNA break was examined by gel electrophoresis. The cell cycle, apoptosis index (AI) and the expression of apoptosis associated gene were analysed by flow cytometry.

Results: 0.5 microgram/ml Tanshinone II A could induce the apoptosis of CNE-1 cells. In the treatment group, the morphologic characteristics of apoptotic cells were observed, the DNA of cells presented "ladder" break, the cell growth and proliferation were inhibited obviously, and the AI was 16.9% (the AI of control group was 6.4%). The cells were arrested in G0/G1 phase and cellular DNA synthesis was inhibited. The expressions of apoptosis associated gene fas, bax, p53 and p21 were up-regulated; the expression of bcl-2 was down-regulated.

Conclusion: Tanshinone II A can induce apoptosis of human nasopharyngeal carcinoma cells. Its molecular mechanism may relate to modulation of the apoptosis associated gene expression.

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