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二肽基肽酶-IV介导内皮间质转化在糖尿病肾纤维化过程中的作用及机制研究

宋丽 孙玉红 施森

泸州医学院学报Issue(1):21-25,5.
泸州医学院学报Issue(1):21-25,5.DOI:10.3969/j.issn.1000-2669.2016.01.002

二肽基肽酶-IV介导内皮间质转化在糖尿病肾纤维化过程中的作用及机制研究

Effect and mechanisms of dipeptidyl peptidase-IV on endothelial-to-mesenchymal transition in diabetic kidney fibrosis

宋丽 1孙玉红 2施森3

作者信息

  • 1. 四川医科大学附属第一医院麻醉科,四川泸州 646000
  • 2. 四川医科大学附属第一医院药理学教研室,四川泸州 646000
  • 3. 四川医科大学附属第一医院附属医院血管外科,四川泸州 646000
  • 折叠

摘要

Abstract

Objective To analyze the roles and mechanisms of dipeptidyl peptidase-IV (DPP-IV) on endothelial-to-mesenchymal transition in diabetic kidney fibrosis. Methods Diabetic CD1 mice were used as chronic diabetic kidney fibrosis model. Mice were treated with or without DPP-IV inhibitor for 4 weeks, kidney samples from each groups were used to analyze the pathological changes, DPP-IV protein levels, and endothelial-to-mesenchymal transition. In vitro, human microvascular endothelial cells were stimulated with or without TGFβ2, and after treatment with DPP-IV inhibitor or siRNA, cell migration, DPP-IV protein levels, endothelial-to-mesenchymal transition, and TGFβ/smad signaling were analyzed. Results: Diabetic CD-1 mice exhibited significant kidney fibrosis and high levels of DPP-IV expression when compared with control mice. DPP-IV inhibitor-treated diabetic mice exhibited a suppression of DPP-IV protein expression and an amelioration of kidney fibrosis associated with the inhibition of EndoMT. In cultured endothelial cells, we found that DPP-IV inhibitor inhibited TGFβ2-induced EndoMT and TGFβ/Smad signaling. Conclusion: DPP-IV inhibitor can ameliorate kidney fibrosis by suppressing EndoMT and TGFβ/Smad signaling.

关键词

二肽基肽酶-IV/糖尿病肾纤维化/内皮间质转化

Key words

Dipeptidyl peptidase-IV/Diabetic kidney fibrosis/Endothelial-to-mesenchymal transition

分类

医药卫生

引用本文复制引用

宋丽,孙玉红,施森..二肽基肽酶-IV介导内皮间质转化在糖尿病肾纤维化过程中的作用及机制研究[J].泸州医学院学报,2016,(1):21-25,5.

基金项目

国家自然科学基金项目 ()

泸州医学院学报

2096-3351

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