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目的:研究恩格列净(empagliflozin)对db/db小鼠肾脏损伤的保护作用及其潜在作用机制。方法:db/db小鼠随机分为糖尿病肾病组(db/db组)和恩格列净治疗组(Empa组，恩格列净10 mg·kgn -1·dn -1灌胃)，C57BL/6J小鼠作为正常对照组。干预3个月，检测血清生化、炎症因子等指标；病理染色观察肾脏病理学改变；检测细胞焦亡相关分子NLRP3、Cleaved Caspase-1、GSDMD的蛋白表达水平。n 结果:与db/db组相比，Empa组空腹血糖、HbAn 1C、血脂、血清IL-1β、IL-18及ACR明显降低(均n P<0.05)，病理染色显示Empa组肾小球固缩、肾间质纤维化明显改善，Empa组肾脏组织NLRP3、Cleaved Caspase-1、GSDMD蛋白表达下调(n P<0.05)。n 结论:恩格列净可能通过抑制NLRP3/Caspase-1/GSDMD细胞焦亡信号通路而改善糖尿病小鼠肾脏损伤。“,”Objective:To investigate the effect of empagliflozin on diabetic kidney disease in db/db mice and the potential mechanisms.Methods:db/db mice were randomly divided into db/db group and Empa group. C57BL/6J mice were used as normal control group. We measured the level of serum biochemistry and inflammatory cytokines. Pathological changes of kidney were observed by pathological staining. The protein expression levels of NLRP3, cleaved caspase-1 and GSDMD were detected.Results:Compared with db/db group, the level of fasting blood glucose, blood lipids, serum biochemistry, and urinary protein-to-creatinine ratio in Empa group were significantly decreased (n P<0.05). HE staining and Masson staining showed that empagliflozin could significantly improve glomerular pyknosis and renal interstitial fibrosis in db/db mice. Meanwhile, the expressions of NLRP3, cleaved caspase-1, and GSDMD protein were down-regulated (n P<0.05).n Conclusion:Empagliflozin improves kidney damage in diabetic model mice, and the possible mechanism is to inhibit the cell pyroptosis signal pathway of NLRP3/caspase-1/GSDMD.