期刊
JOURNAL OF GINSENG RESEARCH
卷 38, 期 3, 页码 167-172出版社
KOREAN SOC GINSENG
DOI: 10.1016/j.jgr.2014.04.002
关键词
alcoholic liver disease; Lactobacillus; Panax ginseng; urushiol
资金
- Korea Society of Ginseng
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education, Science, and Technology [NRF-2010-0021482]
- Cooperative Research Program for Agriculture Science and Technology Development [PJ009859]
- Rural Development Administration, Republic of Korea
- Hallym University Research Fund
Background: Roles of immune reaction and toll-like receptor-4 (TLR-4) have widely been established in the pathogenesis of alcoholic liver disease (ALD). Methods: We evaluated the biologic efficacy of Korean Red Ginseng (KRG), urushiol, and probiotics (Lactobacillus rhamnosus R0011 and Lactobacillus acidophilus R0052) in mouse models of ALD. Sixty C57BL/6 mice were equally divided into six feeding groups for 10 weeks: normal diet, alcohol, control, alcohol + KRG, alcohol + urushiol, and alcohol + probiotics. Alcohol was administered via a Lieber-DeCarli liquid diet containing 10% alcohol. TLR-4 expression, proinflammatory cytokines, and histology, as well as the results of liver function tests were evaluated and compared. Results: No between-group differences were observed with regard to liver function. TLR-4 levels were significantly lower in the KRG, urushiol, and probiotics groups than in the alcohol group (0.37 +/- 0.06 ng/mL, 0.39 +/- 0.12 ng/mL, and 0.33 +/- 0.07 ng/mL, respectively, vs. 0.88 +/- 0.31 ng/mL; p < 0.05). Interleukin-1 beta levels in liver tissues were decreased among the probiotics and KRG groups. The tumor necrosis factor-alpha level of liver tissue was decreased in the KRG group. Conclusion: The pathological findings showed that alcohol-induced steatosis was significantly reduced by KRG and urushiol. As these agents improve immunologic capacity, they may be considered in potential anti-ALD treatments. Copyright (C) 2014, The Korean Society of Ginseng, Published by Elsevier. All rights reserved.
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