【摘要】 目的探讨钙激活钾通道（KCa）在纳米SiO₂致脐静脉内皮细胞损伤中的作用。方法人脐静脉内皮细胞EAhy926正常培养为阴性对照组,5、10、20μg/ml纳米SiO2浓度组,又以20μg/ml纳米SiO₂为阳性对照组,在阳性对照组的基础上加入不同浓度的钙激活钾通道阻断剂,测定各组细胞存活率、乳酸脱氢酶（LDH）活力、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）的释放量。结果细胞存活率随着纳米SiO₂浓度的增加而降低,LDH活力、IL-6和IL-8的释放量随着纳米SiO₂浓度的增加而升高。与阳性对照组比较,3种阻断剂均能提高细胞存活率,减少IL-6和IL-8的释放量,差异有统计学意义（P<0.05）,小电导钙激活钾通道（SK）阻断剂还可降低LDH活力。结论阻断钙激活钾通道可使细胞存活率升高,减少炎性因子IL-6和IL-8的释放量,该通道在纳米SiO₂引起的细胞炎性反应的早期发挥一定作用。更多还原

【Abstract】 Objective To study the role of calcium activated-potassium channels（KCa）in nanometer silica（nano-SiO₂）induced cell injury in umbilical vein endothelial cells.Methods Taking the cultured human umbilical vein endothelial cells as negative control,the co-cultured with 5,10 and 20μg/ml nano-SiO₂ as dose group,20μg/ml nano-SiO₂ as the positive control and together with channels inhibitors as intervention group,at last the cell viability,lactate dehydrogenase（LDH）activity,interleukin-6（IL-6）and interleukin-8（IL-8）production in culture supernatants were detected in all the groups.Results Cell viability decreased with the increasing concentrations of nano-SiO2,LDH activity,IL-6 and IL-8 production increased with the increasing concentrations of nano-SiO₂.Compared to the positive control group,cell viability increased significantly,however,IL-6and IL-8production decreased after adding calcium activated-potassium channels inhibitors（P<0.05）.Small conductance calcium activated-potassium channels inhibition could also decrease the LDH activity.Conclusions Calcium activated-potassium channels inhibitors might increase cell viability,and decrease the production of IL-6,IL-8.Calcium activated-potassium channels played a role in nano-SiO₂ induced the early inflammatory response.更多还原