Akademik Veri Yönetim Sistemi
Archives of Clinical and Experimental Medicine, cilt.6, sa.3, ss.127-133, 2021 (Hakemli Dergi)
Aim: Vitamin D deficiency (VDD) is suggested to enhance hepatotoxicity in chronic liver diseases. However, there is limited knowledge about the association between VDD and alcoholic liver damage. Therefore, the effect of VDD on ethanol (EtOH)-induced hepatotoxicity was investigated in this study. Moreover, the role of the Nrf2-antioxidant signaling pathway in the hepatoprotective potential of 1,25(OH)2D3 was also searched in EtOH-treated rats. Methods: Male Wistar rats were fed on VDD-diet for 12 weeks. EtOH (5-20%) was applied in drinking water in increasing concentrations for the last 8 weeks. In addition, one group of rats were injected with 1,25(OH)2D3 (5μg/kg; twice a week; i.p.) during this period. Hepatic triglyceride and hydroxyproline levels, inflammation markers, lipid peroxides, protein carbonyls, mRNA expressions of Nrf2, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), SOD and GSH-Px activities, glutathione levels and histopathology were examined. Results: EtOH application caused steatosis and fibrosis, elevated hepatic TG, lipid peroxide, protein carbonyls and hydroxyproline levels and inflammation markers. VDD did not aggravate EtOH-induced liver damage, steatosis and inflammation, but reactive oxygen species and lipid peroxide levels were slightly increased in VDD+EtOH group. Gene expressions of Nrf2-SOD-GSH-Px, enzyme activities and glutathione levels were also higher in VDD+EtOH group than EtOH group. Additionally, 1,25(OH)2D3 elevated mRNA expressions and activities of SOD and GSH-Px in EtOH-treated rats. Conclusion: Our results indicate that VDD diet did not cause an additive effect on EtOH-induced hepatotoxicity. Moreover, it was detected that the activation of Nrf2-antioxidant signaling pathway may play a role in the protective effect of 1,25(OH)2D3 against EtOH-induced hepatotoxicity.