Magnolia officinalis Reverses Alcoholic Fatty Liver by Inhibiting the Maturation of Sterol Regulatory Element–Binding Protein-1c

Hu-Quan Yin; Young-Tae Je; Young-Chul Kim; Young-Kee Shin; SangHyun Sung; KiYong Lee; Gil-Saeng Jeong; Youn-Chul Kim; Byung-Hoon Lee

doi:10.1254/jphs.08182FP

Full Papers

Magnolia officinalis Reverses Alcoholic Fatty Liver by Inhibiting the Maturation of Sterol Regulatory Element–Binding Protein-1c

Hu-Quan Yin, Young-Tae Je, Young-Chul Kim, Young-Kee Shin, SangHyun Sung, KiYong Lee, Gil-Saeng Jeong, Youn-Chul Kim, Byung-Hoon Lee

Author information

Hu-Quan Yin
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea
Young-Tae Je
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea
Young-Chul Kim
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea
Young-Kee Shin
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea
SangHyun Sung
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea
KiYong Lee
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea
Gil-Saeng Jeong
College of Pharmacy, Wonkwang University, Korea
Youn-Chul Kim
College of Pharmacy, Wonkwang University, Korea
Byung-Hoon Lee
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Korea

Keywords: Magnolia officinalis, alcoholic fatty liver, tumor necrosis factor-α (TNF-α), reactive oxygen species, sterol regulatory element–binding protein (SREBP)

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Supplementary material

2009 Volume 109 Issue 4 Pages 486-495

DOI https://doi.org/10.1254/jphs.08182FP

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Abstract

The generally accepted hypothesis for the pathogenesis of alcoholic liver disease (ALD) is the two-hit model, which proposes that fat accumulation in the liver increases the sensitivity of the liver to a second hit that leads to inflammatory liver cell damage. In this study we evaluated the effects of Magnolia officinalis (MO), which contains honokiol and magnolol as the primary pharmacological components, to eradicate fatty liver in rats fed an ethanol diet. In vitro studies showed that MO was able to protect RAW 264.7 cells from ethanol-induced production of tumor necrosis factor-α, reactive oxygen species, and superoxide anion radicals; the activation of NADPH oxidase; and subsequent cell death. We also investigated the therapeutic effects of MO on alcoholic fatty liver in Lieber-DeCarli ethanol diet–fed rats. MO treatment of the rats for the last 2 weeks of ethanol feeding completely reversed all the serum, hepatic parameters, and fatty liver changes. The increased maturation of sterol regulatory element–binding protein-1c in the liver by ethanol treatment was completely inhibited by treatment with MO. Therefore, MO may be a promising candidate for development as a therapeutic agent for ALD.

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