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http://dx.doi.org/10.15188/kjopp.2018.08.32.4.226

Protective Effects of Chijabaegpi-tang on Atopic Dermatitis in TNF-α/IFNγ-induced HaCaT Cells  

Eun, So Young (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Yoon, Jung Joo (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Kim, Hye Yoom (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Ahn, You Mee (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Han, Byung Hyuk (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Hong, Mi Hyeon (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Son, Chan Ok (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Na, Se Won (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Lee, Yun Jung (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Kang, Dae Gill (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Lee, Ho Sub (Department of Phygiology, College of Korean Medicine, Wonkwnag University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.32, no.4, 2018 , pp. 226-231 More about this Journal
Abstract
Chijabaegpi-tang (CHG) is an oriental herbal medicine that has been used for its various pharmacological effects, which include anti-inflammatory, anti-oxidant and immunoregulation activities. In the present study, we investigated which skin inflammations are involved in the $TNF-{\alpha}/IFN{\gamma}$-induced HaCaT cells. We investigated the suppressive effect of CHG on $TNF-{\alpha}/IFN{\gamma}$-induced HaCaT cell production of the following chemokines: macrophage-derived chemokine (MDC)/CCL22; regulated on activation, normal T-cell expressed and secreted (RANTES)/CCL5; and interleukin-8 (IL-8); thymus and activation-regulated chemokine (TARC)/CCL17. The pre-treatment of HaCaT cells with CHG suppressed $TNF-{\alpha}/IFN{\gamma}$-induced nuclear transcription factor kappa-B ($NF-{\kappa}B$). In addition, CHG inhibited $TNF-{\alpha}/IFN{\gamma}$-induced phosphorylation of ERK and p38. $TNF-{\alpha}/IFN{\gamma}$ suppressed the expression of skin barrier proteins, including filaggrin (FLG), Involucrin (IVL) and loricrin (LOR). By contrast, CHG restored the expression of FLG, IVL and LOR. Taken together, our findings suggest that CHG could be a therapeutic agent for prevention of skin disease, including atopic dermatitis.
Keywords
Chijabaegpi-tang; Skin inflammation; HaCaT; Atopic dermatitis;
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