Chrysin inhibits diabetes‐associated renal fibrosis through blocking epithelial to mesenchymal transition in tubular epithelial cells under high glucose episode (829.17)

Abstract

Renal fibrosis is a crucial process in the pathogenesis of diabetic nephropathy (DN). This process, known as epithelial to mesenchymal transition (EMT), contributes to the renal accumulation of matrix proteins, where renal tubular epithelial cells play an important role in progressive renal fibrosis. The current study investigated that chrysin (5,7‐dihydroxyflavone), a flavonoid present in bee propolis and herbs, inhibited renal EMT and fibrosis followed by chronic hyperglycemia. Human renal proximal epithelial cells were exposed to 5.5 mM or 33 mM glucose in the absence and presence 1‐20 μM chrysin for 72 h. Mannitol was employed as an osmotic control. Chrysin significantly inhibited renal EMT process through blocking high glucose (HG)‐induced expression of the mesenchymal markers vimentin and α‐smooth muscle actin in renal tubular cells. HG enhanced E‐cadherin expression in tubular cells and retarded N‐cadherin induction, which was reversed by chrysin. In addition, chrysin effectively deterred the excessive deposition of extracellular matrix components of collagen IV and connective tissue growth factor by HG, indicating the blockade of renal fibrosis resulting from myofibroblasts after HG episode. These results demonstrate that chrysin inhibits EMT‐ mediated renal tubular fibrosis due to chronic hyperglycemia. Therefore, chrysin may be a potent renoprotective agent for the treatment of DN.