Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction

Previous studies have demonstrated the potential antifibrotic effects of baicalin invitro, via examination of 21 compounds isolated from plants. However, its biological activity and underlying mechanisms of action invivo remain to be elucidated. The present study aimed to evaluate the effect of baicalin on renal fibrosis in vivo, and the potential signaling pathways involved. A unilateral ureteral obstruction (UUO)-induced renal fibrosis model was established using Sprague-Dawley rats. Baicalin was administrated intraperitoneally every 2days for 10days. The degree of renal damage and fibrosis was investigated by histological assessment, and detection of fibronectin and collagenI mRNA expression levels. Epithelial-mesenchymal transition (EMT) markers, transforming growth factor-beta 1 (TGF-beta 1) levels and downstream phosphorylation of mothers against decapentaplegicy 2/3 (Smad2/3) were examined invivo and in an NRK-52E rat renal tubular cell line invitro. Baicalin was demonstrated to markedly ameliorate renal fibrosis and suppress EMT, as evidenced by reduced interstitial collagen accumulation, decreased fibronectin and collagen I mRNA expression levels, upregulation of N-yandE-cadherin expression levels, and downregulation of alpha-smooth muscle actin and vimentin expression. Furthermore, baicalin decreased TGF-beta 1 expression levels in serum and kidney tissue following UUO, and suppressed Smad2/3 phosphorylation in rat kidney tissue. Invitro studies identified that baicalin may inhibit the phosphorylation of Smad2/3 under the same TGF-beta 1 concentration. In conclusion, baicalin may protect against renal fibrosis, potentially via inhibition of TGF-beta 1 production and its downstream signal transduction.