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MiR-200a抑制Wnt/β-catenin信号通路缓解肾间质纤维化

陈华 龚艺 周宝尚 张璟

中国临床药理学与治疗学2017,Vol.22Issue(4):381-386,6.
中国临床药理学与治疗学2017,Vol.22Issue(4):381-386,6.

MiR-200a抑制Wnt/β-catenin信号通路缓解肾间质纤维化

MiR-200a alleviates renal interstitial fibrosis by inhibiting Wnt/β-catenin signaling pathway

陈华 1龚艺 1周宝尚 1张璟1

作者信息

  • 1. 第三军医大学新桥医院肾内科,重庆400037
  • 折叠

摘要

Abstract

AIM:To investigate the inhibition of miR-200a on Wnt/β-catenin signaling pathway in unilateral ureteral obstruction mouse,and the effects of miR-200a on renal interstitial fibrosis.METHODS:Models of renal interstitial fibrosis were established by unilateral ureteral obstruction (UUO).Twenty-four six-weeks C57BL/6 male mice were randomly divided into four groups (n =6),Sham group,UUO group,UUO + miR-200a group and UUO + NC group.From day 1,UUO + miR-200a group was given miR-200a (i.v.by tail vein,40mg/kg),while UUO + NC group was given Negative Control (i.v.by tail vein,40 mg/kg).Both groups were administered for three consecutive days.On day 7,HE and Masson staining were used to detect pathological changes in kidneys;RT-PCR and Western blot were used to detect mRNA and protein expressions of Wnt4,β-catenin,Fibronectin and α-SMA.RESULTS:Compared with Sham group,UUO group exhibited obvious renal tubular damage and interstitial collagen deposition;expressions of Wnt4,β-catenin,Fibronectin and α-SMA mRNAs and proteins were also increased in UUO group (P <0.05).Compared with UUO group,UUO + miR-200a group presented minor renal tubular injury and interstitial collagen deposition;expressions of Wnt4,β-catenin,Fibronectin α-SMA mRNAs and proteins were also reduced in UUO + miR-200a group (P <0.05).CONCLUSION:miR-200a can alleviate renal interstitial fibrosis by inhibiting the Wnt/β-catenin signaling pathway.

关键词

miR-200a/Wnt/β-catenin信号通路/肾间质纤维化

Key words

miR-200a/Wnt/β-catenin signaling pathway/renal interstitial fibrosis

分类

医药卫生

引用本文复制引用

陈华,龚艺,周宝尚,张璟..MiR-200a抑制Wnt/β-catenin信号通路缓解肾间质纤维化[J].中国临床药理学与治疗学,2017,22(4):381-386,6.

基金项目

国家自然科学基金项目(81270775) (81270775)

中国临床药理学与治疗学

OACSCDCSTPCD

1009-2501

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