Ningning Li 1 , Jinzhong Zhang 2 , Tao Sun 3 , Yanfei Lei 4 , Xianghua Liu 5 , Zhenzhen Li 6 Show Affiliations »
Abstract
AIMS: The purpose of this study was to investigate the influences of apigenin on proliferation, differentiation and function of renal fibroblast after TGF-β1 stimulation and to uncover the underlying mechanisms. BACKGROUND: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. OBJECTIVE: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. METHOD: Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 µM) followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed. RESULT: As a consequence, apigenin alleviated fibroblast proliferation and fibroblast-myofibroblast differentiation induced by TGF-β1. Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased phosphorylation of AMP-activated protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts. CONCLUSION: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced of ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
AIMS: The purpose of this study was to investigate the influences of apigenin on proliferation, differentiation and function of renal fibroblast after TGF-β1 stimulation and to uncover the underlying mechanisms. BACKGROUND: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease . Activated fibroblasts contribute remarkably to the development of renal fibrosis . Although apigenin has been demonstrated to play a protective role from fibrotic diseases , its pharmacological effect on renal fibroblast activation remains largely unknown. OBJECTIVE: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. METHOD: Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 µM) followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis -associated genes in renal fibroblasts was assessed. RESULT: As a consequence, apigenin alleviated fibroblast proliferation and fibroblast-myofibroblast differentiation induced by TGF-β1. Notably, apigenin significantly inhibited the fibrosis -associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased phosphorylation of AMP-activated protein kinase (AMPK ). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3 , p38 and JNK MAPK in renal fibroblasts. CONCLUSION: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced of ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis . Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities: CellLine
Disease
Gene
Keywords:
AMP-activated protein kinase; Apigenin; ERK; TGF-β1; renal fibroblast
Year: 2020
PMID： 32196447 DOI： 10.2174/1389201021666200320140908
Source DB: PubMed Journal: Curr Pharm Biotechnol ISSN： 1389-2010 Impact factor: 2.837