Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways.

Baicalein is a natural flavonoid that possesses notable anti-inflammatory effects. In this study, we detected whether baicalein protects against inflammatory response in unilateral ureteral obstruction mice model to ameliorate tubulointerstitial fibrosis. Baicalein treatment significantly attenuated tubulointerstitial fibrosis by markedly reducing fibronectin and collagen-I. The downregulation of alpha-smooth muscle actin and upregulation of E-cadherin indicated that the epithelial-mesenchymal transition process was suppressed. Furthermore, baicalein administration blocked the infiltration of macrophages and lymphocytes, as evidenced by the significantly reduced CD68 and CD3 positive cells. Meanwhile, the mRNA expression of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein in baicalein-treated groups was markedly reduced compared with the vehicle-treated group. More importantly, unilateral ureteral obstruction induced the activation of NF-κB and mitogen-activated protein kinase signal pathways to switch on inflammatory response to aggravate kidney fibrosis, but these effects were mitigated by baicalein. These data demonstrate that baicalein could inhibit inflammatory process via inactivation of NF-κB and MAPK signal pathways to execute its anti-fibrotic actions in obstructive kidney disease.