Attenuation of Age-Related Hepatic Steatosis by Dunaliella salina Microalgae in Senescence Rats through the Regulation of Redox Status, Inflammatory Indices, and Apoptotic Biomarkers. (1st May 2020) - El-Baz, Farouk K.
Abstract : Background . Hepatic steatosis is the most common type of chronic liver disease and is considered an established risk factor of major chronic diseases. Purpose . The present study aimed to investigate the effect of Dunaliella salina, a microalga and its isolated zeaxanthin on age-related hepatic steatosis as well as their underling mechanism. Study Design . Age-related hepatic steatosis was induced in rats by intraperitoneal injection of D-galactose (200 mg/kg/day) for eight consecutive weeks. D. salina biomass (BDS; 450 mg/kg), its polar fraction (PDS; 30 mg/kg), carotenoid fraction (CDS; 30 mg/kg), and isolated zeaxanthin heneicosylate (ZH; 250 μ g/kg) were orally administered to D-galactose treated rats for two weeks. Methods . Blood samples were collected 24 hours after the last dose of D. salina treatments, animals were sacrificed, and liver tissues were isolated. Sera as well as hepatic tissue homogenates were used for further investigations. Liver tissues were also used for histopathological and immunohistochemical examinations. A computed virtual docking study for the biologically active candidates was performed to confirm the proposed mechanism of action. Results . Oral treatment of D-galactose-injected rats with BDS, PDS, CDS, or ZH ameliorated the serum hepatic function parameters as well as serum levels of adiponectin, apolipoprotein B 100, and insulin. Furthermore, D. salina decreased the hepatic lipid contents, redox status biomarkers, inflammatory cytokine, and showing antiapoptotic properties. Molecular docking of β -carotene and zeaxanthin on various receptors involved in the pathophysiological cascade of steatosis highlighted the possible mechanism underlying the observed therapeutic effect. Conclusion . D. salina carotenoids have beneficial effect on age-related hepatic steatosis in senescence rats through the regulation of redox status, inflammatory indices, and apoptotic biomarkers.