氯通道在三氧化二砷诱导鼻咽癌细胞凋亡中的作用

发布时间：2018-06-23 00:20

本文选题：氯通道 + 三氧化二砷　；参考：《中国病理生理杂志》2017年04期

【摘要】：目的:探讨氯通道在三氧化二砷(arsenic trioxide,As_2O_3)诱导人鼻咽癌CNE-2Z细胞凋亡中的作用。方法:采用流式细胞术检测CNE-2Z细胞经As_2O_3作用24及48 h的凋亡率;应用膜片钳技术记录As_2O_3激活的细胞膜电流,并分析其电流特性;采用流式细胞术检测氯通道阻断剂DIDS对As_2O_3诱导的CNE-2Z细胞凋亡的抑制作用。结果:(1)5μmol/L As_2O_3能够时间依赖性地诱导的CNE-2Z细胞凋亡;(2)CNE-2Z细胞外灌流含5μmol/L As_2O_3的等渗溶液能够激活一个具有外向整流特征的电流,激活的电流无明显的时间及电压依赖性失活,翻转电位接近氯平衡电位;(3)As_2O_3激活的电流能够被氯通道阻断剂DIDS和NPPB完全抑制,细胞外灌流47%的高渗溶液能够完全抑制As_2O_3激活的电流;(4)氯通道阻断剂DIDS能够抑制As_2O_3诱导的CNE-2Z细胞凋亡。结论:As_2O_3可以激活CNE-2Z细胞的容积敏感性氯通道。氯通道在As_2O_3诱导的CNE-2Z凋亡中发挥重要作用。
[Abstract]:Aim: to investigate the role of chloride channel in the apoptosis of human nasopharyngeal carcinoma (NPC) CNE-2Z cells induced by arsenic trioxide (arsenic trioxide). Methods: flow cytometry was used to detect the apoptosis rate of CNE-2Z cells exposed to As2O3 for 24 h and 48 h, and patch clamp technique was used to record the membrane currents activated by As2O3, and to analyze the current characteristics of CNE-2Z cells. The inhibitory effect of chloride channel blocker Dids on the apoptosis of CNE-2Z cells induced by As2O3 was detected by flow cytometry. Results: (1) 5 渭 mol / L as _ 2O _ 3 could induce apoptosis of CNE-2Z cells in a time-dependent manner, (2) the isosmotic solution containing 5 渭 mol / L as _ 2O _ 3 in CNE-2Z cells could activate an outward rectifying current, and the activated current had no time-and voltage-dependent inactivation. The reversal potential was close to the chlorine equilibrium potential; (3) the current activated by as _ 2O _ 3 could be completely inhibited by the chloride channel blockers Dids and NPPB. Extracellular perfusion of 47% hypertonic solution could completely inhibit the current activated by As2O3, (4) Dids, a chloride channel blocker, could inhibit the apoptosis of CNE-2Z cells induced by Ass _ 2O _ 3. Conclusion the volume-sensitive chloride channel of CNE-2Z cells can be activated by 1% AsS _ 2 O _ 3. Chloride channel plays an important role in the apoptosis of CNE-2Z induced by Ass _ 2O _ 3.
【作者单位】：暨南大学基础医学院生理学系;暨南大学基础医学院药理学系;
【基金】：国家自然科学基金资助项目(No.81272223;No.81273539) 教育部基金项目(No.20124401110009) 广东省科技计划项目(No.2013B051000059) 广东省自然科学基金资助项目(No.2016A030313495) 高水平大学建设医学团组项目(No.88015306010;No.88016013041)
【分类号】：R739.63

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