Ginsenoside Rh2 Ameliorates Atopic Dermatitis in NC/Nga Mice by Suppressing NF-kappaB-Mediated Thymic Stromal Lymphopoietin Expression and T Helper Type 2 Differentiation

Autor: Jun Hyoung Lee, Sun Chang Kim, Chang-Hao Cui, Sungjoo Park, Eunsu Ko, Jingang Hou, Myung Ho Kim
Rok vydání: 2019
Předmět:
CD4-Positive T-Lymphocytes
Male
0301 basic medicine
Thymic stromal lymphopoietin
Ginsenosides
Down-Regulation
ginsenoside
ginseng
Immunoglobulin E
Article
Catalysis
Cell Line
Dermatitis
Atopic
Proinflammatory cytokine
Inorganic Chemistry
Pathogenesis
Mice
03 medical and health sciences
Th2 Cells
0302 clinical medicine
Immune system
thymic stromal lymphopoietin
Dinitrochlorobenzene
Animals
Humans
Interleukin 8
Physical and Theoretical Chemistry
Molecular Biology
Spectroscopy
Skin
NF-κB pathway
Th2 differentiation
atopic dermatitis
biology
Chemistry
Organic Chemistry
NF-kappa B
Cell Differentiation
General Medicine
In vitro
Computer Science Applications
Disease Models
Animal
030104 developmental biology
030220 oncology & carcinogenesis
biology.protein
Cancer research
Cytokines
Tumor necrosis factor alpha
Zdroj: International Journal of Molecular Sciences
Volume 20
Issue 24
ISSN: 1422-0067
Popis: Ginsenosides are known to have various highly pharmacological activities, such as anti-cancer and anti-inflammatory effects. However, the search for the most effective ginsenosides against the pathogenesis of atopic dermatitis (AD) and the study of the effects of ginsenosides on specific cytokines involved in AD remain unclear. In this study, ginsenoside Rh2 was shown to exert the most effective anti-inflammatory action on thymic stromal lymphopoietin (TSLP) and interleukin 8 in tumor necrosis factor-alpha and polyinosinic: polycytidylic acid induced normal human keratinocytes by inhibiting proinflammatory cytokines at both protein and transcriptional levels. Concomitantly, Rh2 also efficiently alleviated 2,4-dinitrochlorobenzene-induced AD-like skin symptoms when applied topically, including suppression of immune cell infiltration, cytokine expression, and serum immunoglobulin E levels in NC/Nga mice. In line with the in vitro results, Rh2 inhibited TSLP levels in AD mice via regulation of an underlying mechanism involving the nuclear factor &kappa
B pathways. In addition, in regard to immune cells, we showed that Rh2 suppressed not only the expression of TSLP but the differentiation of naï
ve CD4+ T-cells into T helper type 2 cells and their effector function in vitro. Collectively, our results indicated that Rh2 might be considered as a good therapeutic candidate for the alternative treatment of AD.
Databáze: OpenAIRE
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