Lee Byung-Hwan, Kim Ho-Kyoung, Jang Minhee, Kim Hyeon-Joong, Choi Sun-Hye, Hwang Sung-Hee, Kim Hyoung-Chun, Rhim Hyewhon, Cho Ik-Hyun, Nah Seung-Yeol
Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University.
Mibyeong Research Center, Korea Institute of Oriental Medicine.
Biol Pharm Bull. 2017;40(7):1063-1070. doi: 10.1248/bpb.b17-00124.
Ginseng extract has been used for prevention of atopic dermatitis (AD) in experimental animal models. However, little is known about its active ingredients and the molecular mechanisms underlying its anti-AD effects. Recently, we isolated a unique lysophosphatidic acid (LPA) receptor ligand, gintonin, from ginseng. Gintonin, the glycolipoprotein fraction of ginseng, contains LPAs, mainly LPA C with other minor lysophospholipid components. A line of evidence showed that serum autotaxin (ATX) activity and level are significantly elevated in human AD patients compared to those in normal controls, which indicates that ATX may be involved in human AD. In a previous study, we demonstrated that gintonin exerted anti-inflammatory effects via inhibition of microglial activation and proinflammatory cytokine production by immune cells and that it strongly inhibited ATX activity. In this study, we investigated whether oral administration of the gintonin-enriched fraction (GEF) could ameliorate the symptoms of 2,4-dinitrofluorobenzene (DNFB)-induced AD in NC/Nga mice. We found that oral administration of GEF to DNFB-induced AD mice for 2 weeks reduced ear swelling and AD skin index. In addition, oral administration of GEF reduced the serum levels of immunoglobulin E, histamine, interleukin-4, and interferon-γ. Histological examination showed that oral administration of GEF attenuated skin inflammation and significantly reduced eosinophil and mast cell infiltration into the skin. Moreover, oral administration of GEF not only decreased serum ATX level but also reduced serum ATX activity. The present study shows that the anti-AD effects of ginseng might be attributed to GEF-induced anti-inflammatory activity and ATX regulation.
人参提取物已被用于在实验动物模型中预防特应性皮炎（AD）。然而，关于其活性成分以及其抗AD作用的分子机制却知之甚少。最近，我们从人参中分离出一种独特的溶血磷脂酸（LPA）受体配体，即人参皂草苷。人参皂草苷作为人参的糖脂蛋白部分，含有溶血磷脂酸，主要是LPA C以及其他少量溶血磷脂成分。一系列证据表明，与正常对照组相比，人类AD患者的血清自分泌运动因子（ATX）活性和水平显著升高，这表明ATX可能与人类AD有关。在先前的一项研究中，我们证明人参皂草苷通过抑制小胶质细胞活化和免疫细胞产生促炎细胞因子发挥抗炎作用，并且它强烈抑制ATX活性。在本研究中，我们调查了口服富含人参皂草苷的组分（GEF）是否能改善2,4-二硝基氟苯（DNFB）诱导的NC/Nga小鼠的AD症状。我们发现给DNFB诱导的AD小鼠口服GEF 2周可减轻耳部肿胀和AD皮肤指数。此外，口服GEF可降低血清免疫球蛋白E、组胺、白细胞介素-4和干扰素-γ的水平。组织学检查显示，口服GEF可减轻皮肤炎症，并显著减少嗜酸性粒细胞和肥大细胞向皮肤的浸润。此外，口服GEF不仅降低血清ATX水平，还降低血清ATX活性。本研究表明，人参的抗AD作用可能归因于GEF诱导的抗炎活性和对ATX的调节。
