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目的研究氯离子通道在阿霉素诱导的低分化鼻咽癌CNE-2Z细胞凋亡及凋亡性容积减小中的作用。方法采用全细胞膜片钳技术记录氯电流,流式细胞术检测细胞凋亡,活细胞图像分析法检测细胞容积变化。结果 (1)阿霉素诱导CNE-2Z细胞凋亡;(2)阿霉素诱导CNE-2Z细胞发生凋亡性容积减小,细胞外灌流阿霉素2 h,细胞容积减小约10%;(3)阿霉素可激活氯通道,产生一个有较明显外向优势的氯电流;(4)氯通道阻断剂5-nitro-2-(3-phenylpropylamino)-benzoate(NPPB)明显抑制阿霉素诱导的凋亡性容积减小、细胞凋亡和氯电流。结论阿霉素可通过激活氯通道而诱导细胞凋亡,氯通道在阿霉素诱导的鼻咽癌细胞凋亡中发挥重要作用。
Objective To investigate the role of chloride channel in adriamycin-induced apoptosis and decrease of apoptotic volume in poorly differentiated nasopharyngeal carcinoma CNE-2Z cells. Methods Whole-cell patch-clamp technique was used to record the chloride current. Flow cytometry was used to detect apoptosis. Cell viability was measured by live cell image analysis. Results (1) Adriamycin induced apoptosis of CNE-2Z cells. (2) Adriamycin induced a decrease in apoptotic capacity of CNE-2Z cells. After adriamycin infusion for 2 h, the cell volume decreased by about 10% ; (3) Doxorubicin activates the chloride channel to produce a chloride current with more obvious extrinsic advantages; (4) Chloride channel blocker 5-nitro-2- (3-phenylpropylamino) -benzoate Inmycin-induced apoptotic volume reduction, apoptosis and chloride current. Conclusion Adriamycin can induce apoptosis through activation of chloride channel. Chloride channel plays an important role in adriamycin-induced apoptosis of nasopharyngeal carcinoma cells.