피부각질세포에서 梔子柏皮湯의 아토피 피부염 개선효과
Protective Effects of Chijabaegpi-tang on Atopic Dermatitis in TNF-α/IFNγ-induced HaCaT Cells
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참고문헌
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초록
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-α/IFNγ-induced HaCaT cells. We investigated the suppressive effect of CHG on TNF-α/IFNγ-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-α/IFNγ-induced nuclear transcription factor kappa-B (NF-κB). In addition, CHG inhibited TNF-α/IFNγ-induced phosphorylation of ERK and p38. TNF-α/IFNγ 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.
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-α/IFNγ-induced HaCaT cells. We investigated the suppressive effect of CHG on TNF-α/IFNγ-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-α/IFNγ-induced nuclear transcription factor kappa-B (NF-κB). In addition, CHG inhibited TNF-α/IFNγ-induced phosphorylation of ERK and p38. TNF-α/IFNγ 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.
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