中文摘要：

目的 探讨容量敏感外向整流性（VSOR）氯通道在H2O2介导系膜细胞凋亡中的作用和可能的机制。方法 全细胞膜片钳技术用于检测VSOR氯电流。细胞凋亡通过吖啶橙／溴化乙锭荧光染色、电子显微镜、TUNEL染色和半胱氨酸天冬氨酸蛋白酶（caspase）-3活性确定。结果 150μmol／L H2O2激活系膜细胞VSOR氯电流，H2O2激活的氯电流具有典型的VSOR氯电流电生理特性，包括：外向整流性、电压依赖性失活。对细胞外高渗透压敏感及被VSOR氯通道阻断剂抑制。VSOR氯通道阻断剂DIDS（100μmol/L），NPPB（10μmol/L）和尼氟灭酸（10μmol/L）明显抑制H2O2介导的系膜细胞凋亡。150μmol H2O2处理2h内，细胞容量明显下降，但这种细胞容量下降被100μmol/L DIDS，10μmol／L NPPB和10μmol／L尼氟灭酸抑制。结论 VSOR氯通道参与H2O2介导的系膜细胞凋亡，其机制与介导凋亡性容量下降有关。

英文摘要：

Objective To investigate the role of volume-sensitive outwardly rectifying （VSOR） chloride channels in mesangial cell apoptosis induced by H2O2. Methods VSOR chloride current was recorded in whole cell configuration. The apoptosis was evaluated by AO/EB staining, transmission electron microscopy, TUNEL staining and caspase-3 activity. Cell volume was measured by Lag-time microphotography. Results Application of 150μmol/L H2O2 led to activation of VSOR Cl^- conductance in mesangial cells. H2O2^-indueed Cl^- current showed phynotypieal properties of VSOR Cl^- channels, including outward rectification, voltage-dependant inactivation at large positive potentials, sensitiveness to hyperosmolarity, inhibition by VSOR Cl^- channel blockers. Moreover, blockage of VSOR Cl^- by DIDS （100μmol/L）, NPPB （10 μmol/L） or niflumic acid （10 Ixmol/L） rescued mesangial cells from H2O2-indueed apoptotie cell death. Treatment for 2 hours with 150μmol/L H2O2 resulted in significant reduction in cell volume. However, the early-phase alterations in cell volume were markedly abolished by pretreatment with VSOR Cl^- channel blockers. Conclusion VSOR Clchannels are involved in H2O2-induced apoptosis of mesangial cells and its mechanism is associated with the decrease of apoptotic volume （AVD）.