Apigenin suppresses mouse peritoneal fibrosis by down-regulating miR34a expression

Area of Science:

• Nephrology
• Cell Biology
• Molecular Biology

Background:

• Peritoneal fibrosis is a serious complication of chronic peritoneal dialysis.
• Effective therapeutic options for peritoneal fibrosis are limited.

Purpose of the Study:

• To investigate the potential of apigenin and microRNA (miRNA) in treating peritoneal fibrosis.
• To evaluate the impact of apigenin on high glucose-induced fibrosis in mouse mesothelial peritoneal cells (MMCs).

Main Methods:

• Induced peritoneal fibrosis in MMCs using high glucose (HG).
• Assessed epithelial-mesenchymal transition (EMT) and apoptosis/autophagy biomarkers via qRT-PCR and Western blotting.
• Quantified miRNA expression, cell viability, and proliferation using qRT-PCR, CCK8 assay, Hoechst staining, and flow cytometry.

Main Results:

• High glucose successfully induced fibrosis in MMCs, altering EMT markers (E-cadherin, TTF, N-cadherin, vimentin).
• miR34a expression was significantly upregulated in HG-induced fibrosis.
• Apigenin treatment decreased miR34a levels and, along with miR34a depletion, promoted MMC proliferation and suppressed apoptosis.

Conclusions:

• Apigenin demonstrates efficacy in inhibiting high glucose-induced peritoneal fibrosis in MMCs.
• The mechanism involves, at least partially, the suppression of miR34a expression.
• Apigenin holds promise as a therapeutic agent for peritoneal fibrosis.