Omega-3 fatty acids alleviate chemically induced acute hepatitis by suppression of cytokines.
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Omega-3 fatty acids alleviate chemically induced acute hepatitis by suppression of cytokines. / Schmöcker, Christoph; Weylandt, Karsten H; Kahlke, Lena; Wang, Jingdong; Lobeck, Hartmut; Tiegs, Gisa; Berg, Thomas; Kang, Jing X.
In: HEPATOLOGY, Vol. 45, No. 4, 4, 2007, p. 864-869.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Omega-3 fatty acids alleviate chemically induced acute hepatitis by suppression of cytokines.
AU - Schmöcker, Christoph
AU - Weylandt, Karsten H
AU - Kahlke, Lena
AU - Wang, Jingdong
AU - Lobeck, Hartmut
AU - Tiegs, Gisa
AU - Berg, Thomas
AU - Kang, Jing X
PY - 2007
Y1 - 2007
N2 - Cytokines such as tumor necrosis factor alpha (TNF-alpha) are key factors in liver inflammation. Supplementation with essential omega-3 polyunsaturated fatty acids (n-3 PUFA) has been demonstrated to lower TNF-alpha and IL-1 production in mononuclear cells. An inflammation-dampening effect has been observed with increased omega-3 fatty acid supplementation in several inflammatory diseases. In this study, we used the transgenic fat-1 mouse, expressing a Caenorhabditis elegans desaturase endogenously forming n-3 PUFA from n-6 PUFA, to analyze the effect of an increased n-3 PUFA tissue status in the macrophage-dependent acute D-galactosamine/lipopolysaccaride (D-GalN/LPS) hepatitis model. We show less severe inflammatory liver injury in fat-1 mice with a balanced n-6/n-3 PUFA ratio as evidenced by reduced serum alanine aminotransferase levels and less severe histological liver damage. This decreased inflammatory response was associated with decreased plasma TNF-alpha levels and with reduced hepatic gene expression of TNF-alpha, IL-1beta, IFN-gamma and IL-6 in fat-1 mice, leading to a decreased rate of apoptosis in livers from fat-1 animals, as measured by DAPI-staining. CONCLUSION: The results of this study offer evidence for an inflammation dampening effect of omega-3 polyunsaturated fatty acids in the context of liver inflammation.
AB - Cytokines such as tumor necrosis factor alpha (TNF-alpha) are key factors in liver inflammation. Supplementation with essential omega-3 polyunsaturated fatty acids (n-3 PUFA) has been demonstrated to lower TNF-alpha and IL-1 production in mononuclear cells. An inflammation-dampening effect has been observed with increased omega-3 fatty acid supplementation in several inflammatory diseases. In this study, we used the transgenic fat-1 mouse, expressing a Caenorhabditis elegans desaturase endogenously forming n-3 PUFA from n-6 PUFA, to analyze the effect of an increased n-3 PUFA tissue status in the macrophage-dependent acute D-galactosamine/lipopolysaccaride (D-GalN/LPS) hepatitis model. We show less severe inflammatory liver injury in fat-1 mice with a balanced n-6/n-3 PUFA ratio as evidenced by reduced serum alanine aminotransferase levels and less severe histological liver damage. This decreased inflammatory response was associated with decreased plasma TNF-alpha levels and with reduced hepatic gene expression of TNF-alpha, IL-1beta, IFN-gamma and IL-6 in fat-1 mice, leading to a decreased rate of apoptosis in livers from fat-1 animals, as measured by DAPI-staining. CONCLUSION: The results of this study offer evidence for an inflammation dampening effect of omega-3 polyunsaturated fatty acids in the context of liver inflammation.
M3 - SCORING: Zeitschriftenaufsatz
VL - 45
SP - 864
EP - 869
JO - HEPATOLOGY
JF - HEPATOLOGY
SN - 0270-9139
IS - 4
M1 - 4
ER -
