Abstract Title:

Apigenin alleviates renal fibroblast activation through AMPK and ERK signaling pathways in vitro.

Abstract Source:

Curr Pharm Biotechnol. 2020 Mar 20. Epub 2020 Mar 20. PMID: 32196447

Abstract Author(s):

Ningning Li, Jinzhong Zhang, Tao Sun, Yanfei Lei, Xianghua Liu, Zhenzhen Li

Article Affiliation:

Ningning Li


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 20µM) 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.

Study Type : Human Study
Additional Links
Pharmacological Actions : Anti-Fibrotic : CK(924) : AC(463)

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Sayer Ji
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