期刊
MOLECULES
卷 23, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/molecules23092236
关键词
TGF-beta 1; Pomolic acid; Renal fibrosis; fibroblast; ECM
资金
- National Research Foundation of Korea grant - Korean Government [NRF-2015R1D1A1A01061026]
Fibrosis is a common pathological feature in most kinds of chronic kidney disease. Transforming growth factor beta 1 (TGF-beta 1) signaling is the master pathway regulating kidney fibrosis pathogenesis, in which mothers against decapentaplegic homolog 3 (SMAD3) with signal transducer and activator of transcription 3 (STAT3) act as the integrator of various pro-fibrosis signals. We examine the effects of pomolic acid (PA) on mice with unilateral ureteral obstruction (UUO) and TGF-beta 1 stimulated kidney fibroblast cells. UUO mice were observed severe tubular atrophy, and tubulointerstitial fibrosis and extracellular matrix (ECM) deposition at seven days postoperatively. However, PA-treated UUO mice demonstrated only moderate injury, minimal fibrosis, and larger reductions in the expression of ECM protein and epithelial-mesenchymal transition (EMT) progress. PA inhibited the SMAD-STAT phosphorylation in UUO mice. PA effects were also confirmed in TGF-beta 1 stimulated kidney fibroblast cells. In this study, we first demonstrated that PA ameliorates fibroblast activation and renal interstitial fibrosis. Our results indicate that PA may be useful as a potential candidate in the prevention of chronic kidney disease.
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