In vitro and in vivo anti-inflammatory activities of Korean Red Ginseng-derived components

被引:103
|
作者
Baek, Kwang-Soo [1 ]
Yi, Young-Su [2 ]
Son, Young-Jin [3 ]
Yoo, Sulgi [1 ]
Sung, Nak Yoon [1 ]
Kim, Yong [1 ]
Hong, Sungyoul [1 ]
Aravinthan, Adithan [4 ]
Kim, Jong-Hoon [4 ]
Cho, Jae Youl [1 ]
机构
[1] Sungkyunkwan Univ, Dept Genet Engn, 2066 Seobu Ro, Suwon 16419, South Korea
[2] Cheongju Univ, Dept Pharmaceut Engn, Cheongju, South Korea
[3] Sunchon Natl Univ, Dept Pharm, Sunchon, South Korea
[4] Chonbuk Natl Univ, Coll Vet Med, Dept Physiol, 79 Gobong Ro, Iksan 54596, South Korea
关键词
anti-inflammatory activity; gastritis; Korean Red Ginseng; nonsaponin fraction; saponin fraction; INFLAMMATION; MECHANISMS; GASTRITIS; SYMPTOMS; EXTRACT; KINASE; SRC;
D O I
10.1016/j.jgr.2016.08.003
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Background: Although Korean Red Ginseng (KRG) has been traditionally used for a long time, its anti-inflammatory role and underlying molecular and cellular mechanisms have been poorly understood. In this study, the anti-inflammatory roles of KRG-derived components, namely, water extract (KRG-WE), saponin fraction (KRG-SF), and nonsaponin fraction (KRG-NSF), were investigated. Methods: To check saponin levels in the test fractions, KRG-WE, KRG-NSF, and KRG-SF were analyzed using high-performance liquid chromatography. The anti-inflammatory roles and underlying cellular and molecular mechanisms of these components were investigated using a macrophage-like cell line (RAW264.7 cells) and an acute gastritis model in mice. Results: Of the tested fractions, KGR-SF (but not KRG-NSF and KRG-WE) markedly inhibited the viability of RAW264.7 cells, and splenocytes at more than 500 mu g/mL significantly suppressed NO production at 100 mu g/mL, diminished mRNA expression of inflammatory genes such as inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-alpha, and interferon-beta at 200 mu g/mL, and completely blocked phagocytic uptake by RAW264.7 cells. All three fractions suppressed luciferase activity triggered by interferon regulatory factor 3 (IRF3), but not that triggered by activator protein-1 and nuclear factor kappa B. Phospho-IRF3 and phospho-TBK1 were simultaneously decreased in KRG-SF. Interestingly, all these fractions, when orally administered, clearly ameliorated the symptoms of gastric ulcer in HCl/ethanol-induced gastritis mice. Conclusion: These results suggest that KRG-WE, KRG-NSF, and KRG-SF might have anti-inflammatory properties, mostly because of the suppression of the IRF3 pathway. Copyright (C) 2016, The Korean Society of Ginseng, Published by Elsevier.
引用
收藏
页码:437 / 444
页数:8
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