氯通道在藤黄酸诱导低分化鼻咽癌细胞凋亡中的作用  

Role of chloride channels in gambogic acid-induced apoptosis of poorly differentiated nasopharyngeal carcinoma cells

作　　者：柏志全[1] 李华荣[1] 张海峰[1] 刘善文[1] 朱林燕[2] 叶文才[3] 陈丽新[2] 王立伟[1] 

机构地区：[1]暨南大学医学院生理学系,广东广州510632 [2]暨南大学医学院药理学系,广东广州510632 [3]暨南大学中药及天然药物研究所,广东广州510632

出　　处：《南方医科大学学报》2011年第8期1304-1308,共5页Journal of Southern Medical University

基　　金：国家自然科学基金(3087056790913020U0932004)~~

摘　　要：目的探讨氯离子通道在藤黄酸诱导低分化鼻咽癌CNE-2Z细胞凋亡过程中的作用。方法采用MTT比色法检测细胞增殖,Hoechst 33342染色法分析细胞凋亡,全细胞膜片钳技术记录氯电流。结果藤黄酸明显抑制CNE-2Z细胞增殖,其抑制作用呈时间和浓度依赖性,IC50为3.1μmol/L;8μmol/L藤黄酸诱导细胞凋亡作用可被氯离子通道阻断剂NPPB和Tamoxifen抑制。藤黄酸诱发CNE-2Z细胞产生一个有明显外向优势的氯电流,可被NPPB明显抑制。结论藤黄酸可能通过激活氯离子通道而诱导CNE-2Z细胞凋亡和抑制细胞增殖,提示氯通道参与藤黄酸诱导的细胞凋亡。Objective To investigate the role of chloride channels in the apoptosis of poorly differentiated nasopharyngeal carcinoma CNE-2Z cells induced by gambogic acid（GA）.Methods MTT assay was applied to detect the proliferation of CNE-2Z cells after GA treatment,and the cell apoptosis was detected by Hoechst 33342 staining.Whole-cell patch clamp technique was employed to record GA-activated Cl-currents in the cells.Results GA inhibited the cell proliferation in a time-and concentration-dependent manner with an IC50 of 3.1 μmol/L for a 48-h treatment.The apoptosis-inducing effect of 8 μmol/L GA was attenuated by the chloride channel blocker NPPB（100 μmol/L） and tamoxifen（20 μmol/L）.GA induced an outward-rectified Cl-current in the cells,which was significantly inhibited by NPPB.Conclusions GA suppresses cell proliferation and induces apoptosis by activating Cl-channels in CNE-2Z cells,suggesting the important role of Cl-channels in GA-induced apoptosis.

关 键 词：藤黄酸 鼻咽癌 细胞凋亡 氯离子通道 膜片钳技术 

分 类 号：R739.6[医药卫生—肿瘤]