Abstract
The aim of this study was to investigate the role of metformin in high glucose-induced mesangial cell proliferation, inflammation and extracellular matrix (ECM) accumulation and to elucidate the underlying mechanism of metformin function. An MTT assay was used to examine rat mesangial cell (RMC) proliferation. The levels of TNF-α, IL-6 and TGF-β in RMCs were determined by ELISA. The protein expression of fibronectin, collagen IV and autophagy-related proteins (Beclin-1, LC3-I and LC3-II) in RMCs was detected using western blot. Fluorescence microscopy analysis was carried out to evaluate RMC autophagy. Our results showed that high glucose-induced RMC proliferation, inflammation and ECM expression, but these effects were markedly reduced by metformin. We confirmed that metformin suppressed high glucose-induced RMC proliferation, inflammation and ECM expression via induction of autophagy. Mechanistic investigation demonstrated an axis of SIRT1-FOXO1 in RMC autophagy. Our data indicated that metformin inhibits high glucose-induced mesangial cell proliferation, inflammation and ECM expression through a SIRT1-FOXO1-autophagy axis.
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