title: Cultivated ginseng inhibits 2,4-dinitrochlorobenzene-induced atopic dermatitis-like skin lesions in NC/Nga mice and TNF-α/IFN-γ-induced TARC activation in HaCaT cells.
abstract: Ginseng contains many bioactive constituents, including various ginsenosides that are believed to have anti-allergic, anti-oxidant, and immunostimulatory activities; however, its effects on atopic dermatitis (AD) remain unclear. In the current study, we hypothesized that cultivated ginseng (CG) would inhibit 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in NC/Nga mice by regulating the T helper (Th)1/Th2 balance. Also, CG inhibits TNF-α/IFN-γ-induced thymus- and activation-regulated chemokine (TARC) expression through nuclear factor-kappa B (NF-κB)-dependent signaling in HaCaT cells. CG ameliorated DNCB-induced dermatitis severity, serum levels of IgE and TARC, and mRNA expression of TARC, TNF-α, IFN-γ, IL-4, IL-5, and IL-13 in mice. Histopathological examination showed reduced thickness of the epidermis/dermis and dermal infiltration of inflammatory cells in the ears. Furthermore, CG suppressed the TNF-α/IFN-γ-induced mRNA expression of TARC in HaCaT cells. CG inhibited TNF-α/IFN-γ-induced NF-κB activation. These results suggest that CG inhibited the development of the AD-like skin symptoms by modulating Th1 and Th2 responses in the skin lesions in mice and TARC expression by suppressing TNF-α/IFN-γ-induced NF-κB activation in keratinocytes, and so may be a useful tool in the therapy of AD-like skin symptoms.
authors: Department of Toxicology, College of Pharmacy, Chungnam National University, Daejeon 305-764, Republic of Korea.
authors: Jae Ho
authors: JH
authors: Choi
authors: Sun Woo
authors: SW
authors: Jin
authors: Bong Hwan
authors: BH
authors: Park
authors: Hyung Gyun
authors: HG
authors: Kim
authors: Tilak
authors: T
authors: Khanal
authors: Hwa Jeong
authors: HJ
authors: Han
authors: Yong Pil
authors: YP
authors: Hwang
authors: Jun Min
authors: JM
authors: Choi
authors: Young Chul
authors: YC
authors: Chung
authors: Sang Kyu
authors: SK
authors: Hwang
authors: Tae Cheon
authors: TC
authors: Jeong
authors: Hye Gwang
authors: HG
authors: Jeong
mesh_terms: D000818:Animals; D002460:Cell Line; D054414:Chemokine CCL17 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D004137:Dinitrochlorobenzene / Q000009:adverse effects*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000494:pharmacology*; D018793:Interleukin-13 / Q000235:genetics / Q000378:metabolism; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism; D015848:Interleukin-5 / Q000235:genetics / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D005894:Panax / Q000737:chemistry*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D012867:Skin / Q000187:drug effects / Q000473:pathology; D058408:Th1-Th2 Balance / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: C106230:CCL17 protein, human; C499538:Ccl17 protein, mouse; D054414:Chemokine CCL17; D004137:Dinitrochlorobenzene; D018793:Interleukin-13; D015848:Interleukin-5; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma