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Vitamin K prevents ethanol‐induced hepatic stellate cell activation.
Author(s) -
KojimaYuasa Akiko,
Suzuura Chie,
MatsuiYuasa Isao
Publication year - 2007
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.21.6.a738-d
Subject(s) - hepatic stellate cell , chemistry , vitamin e , hepatic fibrosis , acetaldehyde , lipid peroxidation , vitamin , fibrosis , malondialdehyde , ethanol , liver injury , medicine , endocrinology , biochemistry , oxidative stress , antioxidant
Fibrosis is a key histologic feature that characterizes the progression of alcohol‐induced hepatic injury in chronic alcohol abusers. Hepatic stellate cells (HSC) are central to the fibrotic response to liver injury as these cells undergo activation with an increase in extracellular matrix deposition during fibrogenesis. Suppression of HSC activation has been proposed as therapeutic strategies for prevention of liver fibrosis. In this study, we investigated the effect of vitamin K on ethanol‐induced activation of hepatic stellate cells. Methods: Isolated HSC were incubated with ethano (EtOH) or acetaldehyde (AcCHO). Type I collagen expression in HSC was detected by immunohistochemistry. Intracellular H 2 O 2 levels were assayed using a fluorimetric method. Malondialdehyde levels were determined as an indicator of lipid peroxidation. The effect of the vitamin K1 and K2 on the response of HSC was also examined. Results: Exposure to EtOH or AcCHO led to increase of collagen synthesis and generate of oxidant stress. These changes were prevented by vitamin K1 and K2. Conclusion: These results suggest that vitamin K has protective effect against ethanol‐induced HSC activation. Vitamin K may be a promising therapeutic means for the management of alcoholic liver diseases.