【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。
【机 构】
：
暨南大学医学院生理学系,暨南大学医学院药理学系,暨南大学中药及天然药物研究所,
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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 channel in gambogic acid-induced apoptosis in poorly differentiated nasopharyngeal carcinoma CNE-2Z cells. Methods Cell proliferation was detected by MTT colorimetric assay. Apoptosis was analyzed by Hoechst 33342 staining. Whole - cell patch clamp technique was used to record the chloride current. Results Gambogic acid significantly inhibited the proliferation of CNE-2Z cells in a time and concentration-dependent manner with an IC50 of 3.1 μmol / L. The apoptosis induced by 8 μmol / L Gambogic acid was inhibited by chloride channel blockers NPPB and Tamoxifen inhibition. Gambogic acid induced CNE-2Z cells to produce a chloride current with obvious extrinsic advantages that could be significantly inhibited by NPPB. Conclusion Gambogic acid can induce apoptosis and inhibit the proliferation of CNE-2Z cells through activation of chloride ion channels, suggesting that chloride channel participates in gambogic acid-induced apoptosis.
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