Abstract
The aim of this study was to evaluate whether: 1) Wnt/β-catenin signaling is involved in cyclosporin A (CsA)-induced hepatotoxicity, and 2) knockdown of this pathway by niclosamide (NCL) attenuate CsA-induced hepatotoxicity. The experiment was accomplished in 21days. Adult male mice were randomly distributed into five groups: control group, CsA (25mg/kg/day) group, CsA+NCL (2.5mg/kg/day) group, CsA+NCL (5mg/kg/day) group, and NCL (5mg/kg/day) group. NCL showed marked hepatoprotection by significantly decreasing liver enzymes activities and ameliorating the histopathological alterations induced by CsA. Besides, NCL alleviated oxidative stress and inflammation. NCL-treated groups (2.5 and 5mg/kg) displayed rise in the expression of hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ) by 2.1- and 2.5-fold, respectively. Notably, NCL (2.5 and 5mg/kg) significantly inhibited Wnt/β-catenin signaling, evidenced by a marked decrease in the hepatic expression of Wnt3a by 54% and 50%, frizzled-7 receptor by 50% and 50%, β-catenin by 22% and 49%, and c-myc by 50% and 50%, respectively. NCL can be regarded as a potential agent to mitigate CsA-induced hepatotoxicity.
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