目的:观察糖肾方对C57BLKS/J db/db(db/db)小鼠肾脏损伤的保护作用,并探讨其机制。方法:8周龄雄性自发性2型糖尿病db/db小鼠与同源不发病db/m小鼠,随机分为正常对照组(db/m组)、模型组(db/db组)、糖肾方给药组(db/db+TSF组),连续喂养12周,记录体质量、肾重、血糖及24h尿白蛋白水平,观察肾脏病理改变,并检测肾组织NADPH氧化酶及Nrf2信号通路表达。结果:与db/m组相比,db/db组小鼠体质量、肾重增加,血糖升高,24h尿白蛋白维持在高水平(P〈0.01),肾小球系膜基质增生;糖肾方干预后可降低db/db小鼠体质量、肾重及24h尿白蛋白水平(P〈0.05,P〈0.01),改善肾组织病理改变,下调肾皮质Nox2、Nox4、p22phox、Nrf2、NQO1表达(P〈0.05,P〈0.01),上调HO-1表达(P〈0.05)。结论:糖肾方对db/db小鼠肾脏具有保护作用,其机制可能与下调NADPH氧化酶表达从而改善氧化损伤有关。
Objective: To observe the renoprotective effect and mechanisms of Tangshen Formula(TSF) on db/db mice. Methods: Eight-week-old male db/db mice and homology db/m mice with spontaneously type 2 diabetes mellitus were divided into normal control group(db/m group), model group(db/db group) and TSF group(db/db+TSF group) and fed for 12 weeks. Body weights, kidney weights, blood glucose levels, 24 h urine protein levels, morphology study and oxidative stress markers were detected. The expression of NADPH oxidase and Nrf2 signal path were detected. Results: Compared with db/m group, the db/db group showed higher body and kidney weights, higher blood glucose levels, higher 24 h urine protein levels(P〈0.01) and severe morphological changes; TSF treatment decreased body weights, kidney weights and 24 h urine protein levels(P〈0.05, P〈0.01), alleviated morphological changes, suppressed the expression of Nox2, Nox4, p22 phox, Nrf2, NQO1(P〈0.05, P〈0.01), upregulated HO-1 expression(P〈0.05). Conclusion: TSF has renoprotective effect on db/db mice, and the mechanism might be related with reducing the expression of NADPH oxidase to suppress oxidative stress.