Tranilast attenuates TGF-β1-induced epithelial-mesenchymal transition in the NRK-52E cells

We previously reported that tranilast can halt the pathogenesis of chronic cyclosporine nephrotoxicity in rats via the transforming growth factor-β (tgf-β) /smad pathway, an important signaling system involved in epithelialmesenchymal transition (emt), but the exact underlying cellular mechanisms are not yet clear. thus, by selecting [0]tgf−β1−induced normal rat kidney proximal tubular epithelial cells (nrk-52e) as a model, we demonstrated potential modifying effect of tranilast on emt-induced by tgf−β1 in vitro. nrk-52e cells were incubated with the blank vehicle (dulbecco’s modified eagle’s medium and f-12 (dmem/f12) added with 10% fetal bovine serum (fbs)), 10 ng/ml tgf-β1 alone or together with 100, 200 or 400μm tranilast for 48 h after incubation in medium containing 1% fbs for 24 h. cell morphological changes were observed to confirm occurrence of emt. protein expressions of two typical markers of emt, e-cadherin and α-smooth muscle actin (α-sma), were assessed by western blotting and flow cytometry, respectively. our results showed that tgf-β1 induced spindle-like morphological transition, the loss of ecadherin protein and upregulation of expression of α-sma. however, the tgf-β1-produced changes in cellular morphology, e-cadherin and α-sma were inversed by tranlilast in concentration-dependent manner. our findings indicate that tranilast can directly inhibit emt. thus, it may be implied that regulation of emt be the target to prevent renal tubulointerstitial fibrosis.