他克莫司通过减少肾小球中血管生成素样蛋白4的表达来治疗膜性肾病
acrolimus reduced glomerular angiopoietin-like-4 to treat membranous nephropathy
目的 膜性肾病是原发性肾病综合征的首要病因之一。目前，膜性肾病的治疗策略具有很多争议。在近期的临床试验中，他克莫司已被证明可以提高膜性肾病患者的缓解率，减少膜性肾病患者的尿蛋白，但是其潜在的机制目前尚不清楚。本实验主要研究他克莫司治疗膜性肾病的机制。方法 建立被动型海曼肾炎模型（PHN）动物模型。PHN大鼠在造模后第7到第28天给予他克莫司（1mg/kg/d）或者等量溶媒。被动型海曼肾炎模型大鼠在第7、14、21和28天处死并分别检测24h尿蛋白含量、血白蛋白、肾小球desmin染色和血管生成素样蛋白4染色。结果 他克莫司可以显著降低PHN大鼠的尿蛋白并使血白蛋白升高。他克莫司可以减少PHN大鼠肾小球中的血管生成素样蛋白4并促进足细胞的修复。结论 在实验性膜性肾病中，他克莫司可以通过减少肾小球中的血管生成素样蛋白4来治疗膜性肾病。
Object Membranous nephropathy (MN) is one of the leading causes of primary nephrotic syndrome. Therapeutic strategies for MN patients are controversial. Tacrolimus has recently been shown to have the added benefit of reducing proteinuria in membranous nephropathy (MN) patients. However, its potential mechanisms remain unknown. Methods: We established passive Heymann nephritis (PHN), a typical animal model of human MN. Rat cohorts were administered tacrolimus or vehicle from days 7 to 28 after the induction of PHN. Results: Tacrolimus treatment markedly reduced glomerular Angptl4, accompanied by a reduction in the established proteinuria and the promotion of podocyte repair. Conclusion: Tacrolimus can reduce glomerular angiopoietin-like-4 to decrease proteinuria in MN.
彭雷、李冰
内科学基础医学药学
膜性肾病他克莫司血管生成素样蛋白4足细胞损伤
Membranous nephropathyTacrolimusangiopoietin-like-4podocyte injury
彭雷,李冰.他克莫司通过减少肾小球中血管生成素样蛋白4的表达来治疗膜性肾病[EB/OL].(2014-06-23)[2025-08-18].http://www.paper.edu.cn/releasepaper/content/201406-336.点此复制
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