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Silymarin Protects HepG2 Cells from Palmitate Induced Cell Death and Interleukin‐8 Production
Author(s) -
Song Ming,
Song Zhenyuan,
Uriarte Silvia,
Chen Theresa,
Deaciuc Ion V,
Lee David,
McClain Craig
Publication year - 2006
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.20.5.lb109-c
Subject(s) - programmed cell death , fatty liver , silybum marianum , nonalcoholic fatty liver disease , medicine , pharmacology , insulin resistance , cirrhosis , liver injury , apoptosis , chemistry , endocrinology , biochemistry , insulin , disease , traditional medicine
BACKGROUND Nonalcoholic steatohepatitis (NASH) is part of the spectrum of nonalcoholic fatty liver disease (NAFLD). About 50% of NASH patients develop liver fibrosis, 15–30% develop cirrhosis, and 3% may progress to liver failure. Elevated serum free fatty acid (FFA) levels may play an etiologic role in NASH, and this is postulated to be a critical link between obesity, insulin resistance and the risk of NASH. Silymarin is a flavonoid, extracted from the milk thistle Silibum marianum . The hepatoprotective properties of silymarin have been reported both from in vitro and in vivo studies, but its possible role in preventing hepatotoxicity from FFA, specifically saturated FFA like palmitate, has not been evaluated. OBJECTIVES We investigated the effects of silymarin on palmitate induced cell death and cytokine (IL‐8) production in hepatocytes. METHODS HepG2 cells were treated with palmitate with or without silymarin. Cell death was measured by DNA fragmentation ELISA and caspase‐3 activity. IL‐8 was assayed by ELISA. RESULTS Silymarin protected HepG2 cells from palmitate induced cell death and the protection was independent of its antioxidant property. Palmitate increased IL‐8 from HepG2 cells and silymarin supplementation prevented this IL‐8 production by palmitate. A caspase‐3 inhibitor also attenuated palmitate induced cell death, but did not prevent palmitate induced IL‐8, suggesting that prevention of IL‐8 production by silymarin was cell death independent. CONCLUSIONS Silymarin may be an effective agent in saturated FFA induced liver injury/inflammation. We postulate that silymarin may have beneficial effects in the treatment of fatty liver disease such as NASH.