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)

서지정보

· 발행기관 : 한의병리학회
· 수록지 정보 : 동의생리병리학회지 / 32권 / 4호 / 226 ~ 231페이지
· 저자명 : 은소영, 윤정주, 김혜윰, 안유미, 한병혁, 홍미현, 손찬옥, 나세원, 이윤정, 강대길, 이호섭

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.

영어초록

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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