BACKGROUND： Bile duct ligation （BDL） and subsequent cholestasis are correlated with oxidative stress, hepatocellular injury and fibrosis. Quercetin is a flavonoid with antifibrotic, and hepatoprotective properties....BACKGROUND： Bile duct ligation （BDL） and subsequent cholestasis are correlated with oxidative stress, hepatocellular injury and fibrosis. Quercetin is a flavonoid with antifibrotic, and hepatoprotective properties. However, the molecular mechanism underlying quercetin-mediated hepatoprotection is not fully understood. The current study was to evaluate mecha- nisms of hepatoprotective effect of quercetin in BDL rat model. METHODS： We divided male Wistar rats into 4 groups （n=8 for each）： sham, sham＋quercetin （30 mg/kg per day）, BDL, and BDL＋quercetin （30 mg/kg per day）. Four weeks later, the rats were sacrificed, the blood was collected for liver enzyme mea- surements and liver for the measurement of Racl, Racl-GTP and NOX1 mRNA and protein levels by quantitative PCR and Western blotting, respectively. RESULTS： Quercetin significantly alleviated liver injury in BDL rats as evidenced by histology and reduced liver enzymes. Furthermore, the mRNA and protein expression of Racl, Racl-GTP and NOX1 were significantly increased in BDL rats compared with those in the sham group （P〈0.05）; quercetin treatment reversed these variables back toward normal （P〈0.05）. Another interesting finding was that the antioxidant markers e.g. superoxide dismutase and catalase were elevated in quercetin-treated BDL rats compared to BDL rats （P〈0.05）. CONCLUSION： Quercetin demonstrated hepatoprotective activity against BDL-induced liver injury through increasing antioxidant capacity of the liver tissue, while preventing the production of Racl, Racl-GTP and NOX1 proteins.展开更多
文摘BACKGROUND： Bile duct ligation （BDL） and subsequent cholestasis are correlated with oxidative stress, hepatocellular injury and fibrosis. Quercetin is a flavonoid with antifibrotic, and hepatoprotective properties. However, the molecular mechanism underlying quercetin-mediated hepatoprotection is not fully understood. The current study was to evaluate mecha- nisms of hepatoprotective effect of quercetin in BDL rat model. METHODS： We divided male Wistar rats into 4 groups （n=8 for each）： sham, sham＋quercetin （30 mg/kg per day）, BDL, and BDL＋quercetin （30 mg/kg per day）. Four weeks later, the rats were sacrificed, the blood was collected for liver enzyme mea- surements and liver for the measurement of Racl, Racl-GTP and NOX1 mRNA and protein levels by quantitative PCR and Western blotting, respectively. RESULTS： Quercetin significantly alleviated liver injury in BDL rats as evidenced by histology and reduced liver enzymes. Furthermore, the mRNA and protein expression of Racl, Racl-GTP and NOX1 were significantly increased in BDL rats compared with those in the sham group （P〈0.05）; quercetin treatment reversed these variables back toward normal （P〈0.05）. Another interesting finding was that the antioxidant markers e.g. superoxide dismutase and catalase were elevated in quercetin-treated BDL rats compared to BDL rats （P〈0.05）. CONCLUSION： Quercetin demonstrated hepatoprotective activity against BDL-induced liver injury through increasing antioxidant capacity of the liver tissue, while preventing the production of Racl, Racl-GTP and NOX1 proteins.
