吡格列酮
体内
SMAD公司
纤维化
下调和上调
肾
内科学
医学
药理学
内分泌学
化学
转化生长因子
生物
糖尿病
2型糖尿病
生物化学
生物技术
基因
作者
Li Sun,Tianhua Xu,Ying Chen,Wei Qu,Dan Sun,Xiaoyu Song,Quan Yuan,Yao Li
出处
期刊:Life Sciences
[Elsevier]
日期:2019-09-01
卷期号:232: 116609-116609
被引量:14
标识
DOI:10.1016/j.lfs.2019.116609
摘要
Pioglitazone has been demonstrated to exert anti-fibrotic and renoprotective effects. But the detailed pharmacological mechanisms have not been clearly revealed. The present study aimed to investigate the possible mechanisms of pioglitazone in these two effects. TGF-β1-stimulated HK-2 cells and unilateral ureteral obstruction (UUO) mice were used as in vitro and in vivo models. The results showed that pioglitazone inhibited Smad-2/3 phosphorylation, upregulated Smad-7 expression and downregulated miR-21-5p expression in TGF-β1-exposed HK-2 cells. In addition, miR-21-5p inhibitors replicated the anti-fibrotic effects of pioglitazone, and miR-21-5p mimics inhibited these effects. In in vivo study, pioglitazone attenuated UUO-induced renal fibrosis and significantly decreased the expressions of pro-fibrotic proteins. Whereas, agomir of miR-21-5p inhibited the renoprotective function of pioglitazone in UUO mice. In conclusion, the present data suggest that modulation of miR-21-5p/Smad-7 signal may be involved in the anti-fibrotic effect of pioglitazone in the kidney of UUO mice.
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