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A novel compound AD021 attenuates renal fibrosis by inhibiting transforming growth factor‐β1 in renal proximal tubule epithelial cells

Renal fibrogenesis is the common final pathway to all renal injuries including injury from diabetes that consequently leads to end‐stage renal disease (ESRD). Currently, there are no potential therapeutic drugs that are both safe and effective to prevent the progression of diabetic nephropathy (DN) patients and eventually ESRD. Transforming growth factor‐β1 (TGF‐β1) as the major player of tubulointerstitial fibrosis induction in diabetic kidneys. Moreover, inhibition of the TGF‐β1 pathway is one of the most effective renal fibrosis therapies in DN. Therefore, we aimed to identify the novel anti‐fibrotic compound using TGF‐β1‐induced fibrosis cells. Renal proximal tubule epithelial cells (RPTEC) were used to evaluate the anti‐fibrotic effect of the natural compounds. Our laboratory has natural and synthetic compounds libraries and some of them have been reported to have beneficial effects in several diseases, but the anti‐fibrotic effect has never been studied. The picro‐sirius red staining and spectrophotometric analysis were used for screening of 335 compounds. The active compound, AD021, effectively inhibited TGF‐β1‐ induced fibrosis in RPTEC cells with IC50 of 11 μM. Profibrotic protein expression levels including fibronectin and α‐smooth muscle actin were decreased in AD021 co‐treatment with TGF‐β1 in a concentration‐dependent manner. Collectively, our findings demonstrated that this novel anti‐fibrotic agent has potential for the development of novel renal fibrosis treatment for DN patients.