Abstract Title:

Apigenin suppresses mouse peritoneal fibrosis by down-regulating miR34a expression.

Abstract Source:

Biomed Pharmacother. 2018 Jun 29 ;106:373-380. Epub 2018 Jun 29. PMID: 29966983

Abstract Author(s):

Yiming Zhang, Qiaoling Sun, Xiang Li, Xiaofen Ma, Yang Li, Zhanfeng Jiao, Xiang-Dong Yang

Article Affiliation:

Yiming Zhang


Peritoneal fibrosis is a severe side-effect of chronic peritoneal dialysis in patients with end-stage renal disease, but not enough effective therapeutic drugs are currently available in clinics. The aim of this study was to evaluate the effects of apigenin and miRNA on the progression of peritoneal fibrosis. We treated isolated mouse mesothelial peritoneal cells (MMCs) with high glucose (HG), to induce fibrosis. We used qRT-PCR and Western blotting to measure the expressions of multiple epithelial-mesenchymal transition (EMT) biomarkers, like E-cadherin, transcription termination factor (TTF), N-cadherin and vimentin, as well as several apoptosis and autophagy biomarkers. We determined the IC50 of apigenin on MMC fibrosis. We also used qRT-PCR to assess the expressions of miRNAs in MMC fibrosis. In addition, we by used the CCK8 assay, Hoechest staining and flow cytometry, to measure cell viability and proliferation rates. We successfully induced fibrosis using high glucose (HG) treatment in MMCs. This was further validated by the observed changes in E-cadherin, TTF, N-cadherin and vimentin expression levels. We also observed highly elevated expression levels of miR34a during HG-induced MMC fibrosis. Apigenin treatment induced a significant decrease in miR34a expression levels in HG-treated MMCs. Moreover, both apigenin treatment and miR34a depletion, as well as their combination, significantly promoted proliferation and suppressed apoptosis of MMCs treated with high glucose. This was accompanied with a corresponding alteration in expressions of EMT, apoptosis and autophagy biomarkers. In summary, apigenin effectively inhibits mouse mesothelial peritoneal cell fibrosis induced by high glucose, and this is, at least partially mediated by the suppression of miR34a expression.

Study Type : In Vitro Study

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