ABSTRACT
PURPOSE: In this study, we investigated the effects of Cirsium setidens ethanolic extract (CS) on the development of alcoholic fatty liver and associated injury. METHODS: Sprague-Dawley male rats were fed either Lieber-DeCarli control (C) or ethanol (35.5% of total calories) liquid diet with 0 (E), 100 mg/kgBW CS (E+LCS), or 500 mg/kgBW CS (E+HCS) for 8 weeks. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as TG and cholesterol concentrations in the serum and liver tissues were measured by colorimetric assays. Liver histopathology was examined by Hematoxylin-eosin staining of the fixed liver tissues. Protein levels of phosphorylated-AMP activated protein kinase (p-AMPK), phosphorylated-acetyl CoA carboxylase (p-ACC), phosphorylated-nuclear factor kappa B (p-NFκB), and TNFα were measured by Western blot analyses. RESULTS: Both doses of CS markedly suppressed alcohol-induced lipid droplets accumulation in the liver tissues and significantly inhibited alcohol-induced increases in activities of serum ALT and serum AST. Similarly, CS significantly reduced hepatic and serum TG concentrations. Compared to groups fed alcohol only, CS supplementation strongly increased hepatic levels of p-AMPK and p-ACC. Further, CS significantly inhibited alcohol-induced phosphorylation of NFκB, which was associated with reduced hepatic protein levels of TNFα. CONCLUSION: Our data demonstrated that CS has a protective effect against alcoholic liver injury, which was associated with activation of AMPK and inhibition of NFκB.
Subject(s)
Animals , Humans , Male , Rats , Alanine Transaminase , Alcoholics , AMP-Activated Protein Kinases , Aspartate Aminotransferases , Blotting, Western , Cholesterol , Cirsium , Diet , Ethanol , Fatty Liver, Alcoholic , Lipid Droplets , Liver , Liver Diseases, Alcoholic , NF-kappa B , Phosphorylation , Protein Kinases , Rats, Sprague-DawleyABSTRACT
In this study, we isolated scopoletin from Cirsium setidens Nakai (Compositae) and tested its effects on melanogenesis. Scopoletin was not toxic to cells at concentrations less than 50 microM and increased melanin synthesis in a dose-dependent manner. As melanin synthesis increased, scopoletin stimulated the total tyrosinase activity, the rate-limiting enzyme of melanogenesis. In a cell-free system, however, scopoletin did not increase tyrosinase activity, indicating that scopoletin is not a direct activator of tyrosinase. Furthermore, Western blot analysis showed that scopoletin stimulated the production of microphthalmia-associated transcription factor (MITF) and tyrosinase expression via cAMP response element-binding protein (CREB) phosphorylation in a dose-dependent manner. Based on these results, preclinical and clinical studies are needed to assess the use of scopoletin for the treatment of vitiligo.