황련-감초 추출물을 이용한 하태독법이 NC/Nga 생쥐에서 유발된 아토피 유사 피부염에 미치는 항염증 효과
Anti-inflammatory Effects of Hataedock Extracted from Coptidis Rhizoma and Glycyrrhiza Uralensis on Atopic Dermatitis-like Skin Lesions of NC/Nga Mouse
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Objectives: Hataedock is an orally administered herbal extract treatment for newborn babies that dispels toxic heat and meconium gathered by the fetus. The purpose of this study was to evaluate whether Hataedock alleviates inflammatory skin damage in AD (Atopic Dermatitis)-induced NC/Nga mice through regulating and maintaining the skin barrier and anti-inflammation effects. Methods: We established an AD model in three-week-old NC/Nga mice through the repeated application of DNFB (dinitrochlorobenzene) on days 28, 35, and 42 after Hataedock treatment was orally administered. We identified changes in the skin barrier and anti-inflammation effects through the histological and immunohistochemical changes of TNF-α, NF-κB p65, iNOS, COX-2, and apoptotic bodies. Results: Skin damage and angiogenesis were mitigated in the HT (Hataedock) group. Damage to the intercellular space of the stratum corneum as well as hyperplasia, edema, the infiltration of lymphocytes, and the increase of capillaries decreased in the HT group. Our results suggest that Hataedock treatment significantly down-regulated levels of TNF-α by 38% (p<0.001) and of NF-κB p65 by 70% (p<0.001). But Hataedock up-regulated apoptosis by 183% in dermatitis-induced skin. Conclusions: These results suggest that Hataedock alleviates AD through diminishing the various inflammatory cytokines in skin lesions that are involved in the initial steps of AD development. It might have potential applications for the prevention and treatment of atopic dermatitis.
Abstract
Objectives: Hataedock is an orally administered herbal extract treatment for newborn babies that dispels toxic heat and meconium gathered by the fetus. The purpose of this study was to evaluate whether Hataedock alleviates inflammatory skin damage in AD (Atopic Dermatitis)-induced NC/Nga mice through regulating and maintaining the skin barrier and anti-inflammation effects. Methods: We established an AD model in three-week-old NC/Nga mice through the repeated application of DNFB (dinitrochlorobenzene) on days 28, 35, and 42 after Hataedock treatment was orally administered. We identified changes in the skin barrier and anti-inflammation effects through the histological and immunohistochemical changes of TNF-α, NF-κB p65, iNOS, COX-2, and apoptotic bodies. Results: Skin damage and angiogenesis were mitigated in the HT (Hataedock) group. Damage to the intercellular space of the stratum corneum as well as hyperplasia, edema, the infiltration of lymphocytes, and the increase of capillaries decreased in the HT group. Our results suggest that Hataedock treatment significantly down-regulated levels of TNF-α by 38% (p<0.001) and of NF-κB p65 by 70% (p<0.001). But Hataedock up-regulated apoptosis by 183% in dermatitis-induced skin. Conclusions: These results suggest that Hataedock alleviates AD through diminishing the various inflammatory cytokines in skin lesions that are involved in the initial steps of AD development. It might have potential applications for the prevention and treatment of atopic dermatitis.
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