熊果酸诱导人乳腺癌细胞MCF-7凋亡的实验研究  

Experimental Study on MCF-7 Cell Apoptosis Induced by Ursolic Acid

作　　者：张维文[1] 黎银燕[1] 张贵平[1] 吕嘉春[1] 区彗坚[1] 

机构地区：[1]广州医学院,广州510182

出　　处：《中药材》2005年第4期297-301,共5页Journal of Chinese Medicinal Materials

摘　　要：目的:探讨三萜类中药成分熊果酸(UrsolicAcid,UA)诱导乳腺癌MCF 7细胞的凋亡作用,从而为开发应用于治疗乳腺癌的药物提供科学依据。方法:应用细胞培养技术,用不同浓度的药物在一定的时间内处理MCF -7细胞,采用MTT法、活细胞原位光镜和荧光染色技术、流式细胞技术(FCM)、荧光免疫组织化学技术,研究药物诱导细胞凋亡引起的形态改变、细胞周期变化、p53蛋白表达。结果:UA剂量依赖性的抑制MCF -7细胞增殖,半数生长抑制剂量(IC50 )为22. 6±3. 0μmol/L,凋亡促进因子p53蛋白表达量增加,有典型的凋亡形态学特征,核质向边缘固缩,有凋亡小体。结论:UA通过抑制MCF -7细胞生长和上调p53的表达诱导细胞凋亡发挥其抗肿瘤细胞的作用。Objective:To study the effects of ursolic acid (UA),apentacyclic triterpene acid,on MCF-7 cell apoptosis.Methods:MCF-7 cells were cultured with different concentrations of UA.Viability of UA-induced MCF-7 cells was evaluated by MTT assay.Cell cycle and sub-G_1 peak were performed by FCM.Morphologic changes of UA-treated cells were observed by light microscope.Apoptotic cells with condensed or fragmented nuclei were visualized by Ho33258 and PI staining by a fluorescence microscope (EX∶U.V.,Green light). p 53 protein expression was analyzed by fluorescence immunohistochemical method (SABC-Cy3).Result:24 hours after UA treatment,inhibition of MCF-7 cell proliferation was concentration-dependent.The IC_ 50 value for UA was 22.6±3.0 μmol/L. Cell cycle analysis by FCM showed that 50 μmol/L of the drug arrested MCF-7 cell cycle at G_0-G_1 phase.Morphological changes of MCF-7 cells exhibited many of the hallmark features of apoptosis,including condensation of chromatin and DNA fragmentation.UA increased p 53 protein expression.Conclusion:The results suggest that UA evokes MCF-7 cell apoptosis is correlation with the up-regulation of p 53. The study indicated that UA might be a potential Chinese medical component for breast neoplasm.

关 键 词：乳腺癌细胞MCF-7 熊果酸 实验研究 MCF-7细胞增殖 免疫组织化学技术 诱导细胞凋亡 p53蛋白表达 细胞培养技术 荧光染色技术 流式细胞技术 剂量依赖性 mol/L 形态学特征 抗肿瘤细胞 中药成分 Acid 凋亡作用 科学依据 药物提供 

分 类 号：R73-36[医药卫生—肿瘤] R284.1[医药卫生—临床医学]