Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells by Inhibiting SmadILKSnail Pathway

Abstract EN

Renal fibrosis is a common cause of renal dysfunction with chronic kidney disease.

Central to this process is epithelial-mesenchymal transformation (EMT) of proximal tubular epithelial cells driven by transforming growth factor-β1 (TGF-β1) signaling.

The present study aimed to investigate the effect of Ferulic acid (FA) on EMT of renal proximal tubular epithelial cell line (NRK-52E) induced by TGF-β1 and to elucidate its underlying mechanism against EMT related to TGF-β1/Smads pathway.

The NRK-52E cells were treated for 48 h with TGF-β1 (5 ng/mL) in different concentrations of FA (0 to 200 µM).

Fibronectin, a mesenchymal marker, was assessed by western blotting.

Western blotting was also used to examine the EMT markers (E-cadherin, and α-smooth muscle actin (α-SMA)), signal transducer (p-Smad2/3), and EMT initiator (Snail).

ILK was also assayed by western blotting.

The results showed that TGF-β1 induced spindle-like morphological transition in NRK-52E cells.

Smad2/3 signaling pathway activation, increased fibronectin, α-SMA, ILK, and Snail expression, and decreased E-cadherin expression in TGF-β1-treated NRK-52E cells.

FA efficiently blocked P-Smad2/3 activation and attenuated all these EMT changes induced by TGF-β1.

These findings suggest that FA may serve as a potential fibrosis antagonist for renal proximal tubule cells by inhibiting EMT process.