Decreased hepatic phosphorylated p38 mitogen-activated protein kinase contributes to attenuation of thioacetamide-induced hepatic necrosis in diet-induced obese mice
Author:
Affiliation:
1. Medicinal Safety Research Laboratories, Daiichi Sankyo Co., Ltd.
Publisher
Japanese Society of Toxicology
Subject
Toxicology
Link
https://www.jstage.jst.go.jp/article/jts/41/2/41_245/_pdf
Reference27 articles.
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3. Calder, P.C. (2009): Polyunsaturated fatty acids and inflammatory processes: New twists in an old tale. Biochimie, 91, 791-795.
4. Cao, W., Daniel, K.W., Robidoux, J., Puigserver, P., Medvedev, A.V., Bai, X., Floering, L.M., Spiegelman, B.M. and Collins, S. (2004): p38 mitogen-activated protein kinase is the central regulator of cyclic AMP-dependent transcription of the brown fat uncoupling protein 1 gene. Mol. Cell. Biol., 24, 3057-3067.
5. Chen, H.W., Lii, C.K., Ko, J.J., Wang, S.T. and Hsu, J.D. (1996): Regulatory effects of dietary n-3 and n-6 lipids on plasma and hepatic lipid levels, liver cell number and microsomal protein content in spontaneously hypertensive rats. Prostaglandins Leukot. Essent. Fatty Acids, 55, 329-335.
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2. Mice in the early stage of liver steatosis caused by a high fat diet are resistant to thioacetamide-induced hepatotoxicity and oxidative stress;Toxicology Letters;2017-08
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