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Hepatoprotective effect of garcinol on dimethylnitrosamine‐induced experimental liver fibrosis
Author(s) -
Cheng AnChin,
Lee MingFen,
Pan MinHsiung,
Tsai Chenyu,
Chen MingDian
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.861.7
Subject(s) - aspartate transaminase , pharmacology , chemistry , alanine transaminase , liver cancer , apoptosis , fibrosis , antioxidant , cancer , smad , cancer research , traditional medicine , medicine , signal transduction , biochemistry , enzyme , alkaline phosphatase
Dietary factors play an important role in human health, which are often associated with the development of chronic diseases, including cancer. Garcinol is a polyisoprenylated benzophenone derivative from Garcinia indica and other related species. Many studies have indicated that garcinol is a pleiotropic agent, whose functions might include antioxidant, scavenger of free radicals, and inhibition of inflammation. Previous studies indicated that garcinol can modulate several cell signaling pathways, including apoptosis and cancer development. This study was to investigate the effect of garcinol on liver fibrosis. Sprague‐Dawley rats were intraperitoneally given dimethylnitrosamine (DMN) (10 mg/kg) three days per week for four weeks. Garcinol (10 or 20 mg/kg) was administered by oral gavage daily. Liver function, morphology, histochemistry, and fibrotic parameters were examined. Garcinol supplementation alleviated the DMN‐induced damage, including the change of the expression levels of alanine transaminase and aspartate transaminase, histopathological status, and multiple fibrotic indexes. These data demonstrated that garcinol exhibited hepatoprotective effects on experimental liver fibrosis, presumably through mediating TGFβ/Smad signaling. This work was supported by the grants, NSC100–2313‐B‐309–003 to An‐Chin Cheng and NSC101–2320‐B‐309–001 to Ming‐Fen Lee, from National Science Council (Taiwan, ROC).