Objective To explore the effect and mechanism of quercetin (QCT) on peritoneal fibrosis (PF) in peritoneal dialysis (PD) rats based on the Wnt / β-catenin pathway. Methods PD rat model was constructed, and successfully modeled rats were stochastically classified into LiCl-N ( LiCl, 0 mg / kg), LiCl-L ( LiCl, 30 mg / kg)、LiCl-M (LiCl, 60 mg / kg), LiCl-H (LiCl, 90 mg / kg), PD, QCT-L (QCT, 17. 5 mg / kg), QCT-H (QCT, 35 mg /kg), and QCT-H+LiCl-M (QCT, 35 mg / kg+LiCl, 60 mg / kg) groups. Another 12 rats served as the Ctrl group.Rats in the Ctrl and PD groups were given an equal amount of 0. 9% sodium chloride solution at the same time and location by gavage once a day for 4 weeks. Peritoneal function was assessed using the peritoneal balance test. Changes in peritoneal tissue were observed by hematoxylin-eosin staining and peritoneal tissue fibrosis was detected by Masson staining. Levels of the inflammatory factors tumor necrosis factor ( TNF)-α, interleukin ( IL)-1β, and IL-6 were detected by enzyme-linked immunosorbent assay. α-smooth muscle actin (SMA), collagen type 1 (CoL-1), and Ecadherin protein levels were detected by immunohistochemistry, and Wnt3a, low-density lipoprotein receptor-related protein 5 (LRP5), lymphoid enhancer-binding factor 1 ( LEF-1), glycogen synthase kinase-(GSK)-3β, and β-catenin proteins were measured by Western blot. Results Compared with the LiCl-N group, rats in the LiCl-L groups showed no effects on serum creatinine ( Scr) and blood urea nitrogen ( BUN) levels, mass transfer of glucose (MTG), ultrafiltration volume (UF), Wnt3a, and β-catenin protein (P>0. 05), Rats in the LiCl-M groups showed same effects, while Wnt3a, β-catenin prote were increased (P<0. 05). Rats in the LiCl-H groups showed more Scr and BUN levels, mass transfer of glucose (MTG), and Wnt3a and β-catenin protein(P<0. 05), while UF were decreased (P<0. 05). Thus, 60 mg / kg was selected as the LiCl concentration. Rats in the PD group shed peritoneal mesothelial cells compared with the Ctrl group’ s number of inflammatory cells, relative area of collagen fiber deposition, peritoneal thickness, Scr and BUN levels, MTG, peritoneal tissue TNF-α, IL-1β, IL-6, α-SMA, CoL-1,Wnt3a, LRP5, LEF-1, and β-catenin were all increased (P<0. 05), while UF, E-cadherin, and GSK-3β proteins decreased (P<0. 05). Compared with the PD group, rats in the QCT-L and QCT-H groups showed less mesothelial cell shedding, number of inflammatory cells, relative area of collagen fiber deposition, peritoneal thickness, SCr,BUN, MTG, peritoneal tissue TNF-α, IL-1β, and IL-6 levels, and α-SMA, CoL-1, Wnt3a, LRP5, LEF-1, and β-catenin proteins were decreased ( P<0. 05), while UF, E-cadherin, and GSK-3β were increased ( P<0. 05).Compared with the QCT-H group, rats in the QCT-H + LiCl-M group showed increased peritoneal tissue damage,increased number of inflammatory cells, relative area of collagen fiber deposition, peritoneal thickness, Scr and BUN levels, MTG, peritoneal tissue TNF-α, IL-1β, and IL-6 levels, and α-SMA, CoL-1, Wnt3a, LRP5, LEF-1, β-catenin proteins (P<0. 05), and decreased UF, E-cadherin, and GSK-3β (P<0. 05). Conclusions QCT alleviates PF in PD rats by inhibiting the inflammatory response and peritoneal mesothelial cell mesenchymal transition process, possibly acting via inhibition of the Wnt / β-catenin signaling pathway.