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目的:探讨百草枯（PQ）染毒肺泡上皮细胞内KCa3.1对NLRP3炎症小体的调控作用。方法:体外培养A549细胞，分为对照组、TRAM-34（KCa3.1的特异性抑制剂）组、PQ组及PQ+TRAM-34组。免疫荧光检测细胞中KCa3.1的变化。Western Blot检测NLRP3炎症小体相关蛋白及NIMA相关激酶7（NEK7）蛋白的表达。细胞钾离子浓度变化比色法定量检测试剂盒检测钾离子的变化。结果:免疫荧光结果提示A549细胞染毒后，KCa3.1表达明显增加。Western Blot结果提示PQ处理后，A549细胞内NLRP3炎症小体（相关蛋白NLRP3、ASC、Caspase-1）及NEK7蛋白表达明显升高；抑制KCa3.1后，NLRP3炎症小体及NEK7表达减少；且差异具有统计学意义[NLRP3蛋白（NLRP3/β-actin，对照组比抑制剂组比染毒组比染毒+抑制剂组）：[(0.02±0.00)n vs (0.03±0.00)n vs （0.74±0.00） n vs （0.32±0.01）]；ASC蛋白（ASC/ β-actin，对照组比抑制剂组比染毒组比染毒+抑制剂组）: [（0.12±0.01）n vs（0.11±0.03）n vs（0.46±0.02）n vs（0.17±0.03）]；Caspase-1蛋白（Caspase-1/ β-actin，对照组比抑制剂组比染毒组比染毒+抑制剂组）:[(0.05±0.00)n vs 0.04±0.00) n vs （0.34±0.03）n vs（0.15±0.01）];NEK7蛋白（NEK7/ β-actin，对照组比染毒组比染毒+抑制剂组）：[(0.38±0.03)n vs （0.83±0.02) n vs (0.51±0.01)，均n P<0.01]。比色法检测结果提示PQ处理后细胞内钾离子明显下降，抑制KCa3.1后细胞内钾离子下降明显减少；且差异有统计学意义（对照组比染毒组比染毒+抑制剂组：[(1.00±0.00)n vs （0.60±0.05）n vs（0.86±0.02），均n P<0.01]。n 结论:PQ中毒后，可能激活KCa3.1促使细胞内钾离子外流，上调NEK7表达，从而激活NLRP3炎症小体，促进肺纤维化的发生。“,”Objective:To explore the effect of KCa3.1 activating NLRP3 inflammasome in paraquat PQ treated-alveolar epithelial cells.Methods:The A549 cells were cultured in vitro and divided into the control group, TRAM-34 (specific inhibitor of KCa3.1) group, PQ group and PQ+TRAM-34 group. The expression of KCa3.1 was detected by immunofluorescence in A549 cells. Western blot was used to detect the level of the proteins related with the NLRP3 infammasome and NEK7 protein. And the level of cell potassium was detected by cell potassium concentration kit.Results:The level of KCa3.1 was significantly increased in A549 cells after PQ treatment by immunofluorescence. The expressions of NLRP3 infammasome-related proteins (NLRP3, ASC and Caspase-1) and NEK7 protein were increased after PQ treatment, and the expressions of NLRP3 infammasome-related proteins and NEK7 protein were decreased after inhibition of KCa3.1, and the difference was statistically significant [NLRP3/β-actin (control groupn vs TRAM-34 group n vs PQ group n vs PQ+TRAM-34 group): [ (0.02±0.00) n vs (0.03±0.00) n vs (0.74±0.00) n vs (0.32±0.01) , ASC/β-actin (control groupn vs TRAM-34 group n vs PQ group n vs PQ+TRAM-34 group): [ (0.12±0.01) n vs (0.11±0.03) n vs (0.46±0.02) n vs (0.17±0.03) ];Caspase-1/ β-actin (control group n vs TRAM-34 group n vs PQ group n vs PQ+TRAM-34 group): [ (0.05±0.00) n vs (0.04±0.00) n vs (0.34±0.03) n vs (0.15±0.01) ]; NEK7/ β-actin (control group n vs PQ group n vs PQ+TRAM-34 group);[ (0.38±0.03) n vs (0.83±0.02) n vs (0.51±0.01) , n P<0.01]. The potassium level was decreased after PQ treatment and the degree could be declined by the KCa3.1 inhibitor by colorimetric detection with statistically significant difference (control group n vs PQ group n vs PQ+TRAM-34 group:[ (1.00±0.00) n vs (0.60±0.05) n vs (0.86±0.02) , n P<0.01].n Conclusions:The KCa3.1 could promote the outflow of intracellular potassium and up-regulate the expression of NEK7, thereby activate the NLRP3 inflammatory in PQ-induced pulmonary fibrosis.