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논문 기본 정보

자료유형
학술저널
저자정보
서일복 (세명대학교) 안상현 (세명대학교) 김기봉 (부산대학교)
저널정보
대한한방소아과학회 대한한방소아과학회지 대한한방소아과학회지 제34권 제4호
발행연도
2020.1
수록면
22 - 30 (9page)

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초록· 키워드

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Objectives: This study was conducted to confirm the inhibitory effect of β-glucan on epithelial inflammation induced by atopic dermatitis through Endocannabinoid system (ECS) activity. Methods: Six-week-old NC/Nga mice were divided into a control group (Ctrl), atopic dermatitis elicitation group (ADE), and a β-glucan-treated group (β-glucan treatment after atopy dermatitis elicitation, β-GT). After 3 weeks, CB1, CB2, and GPR55 were observed to confirm the regulation of ECS activity, and filaggrin in the stratum corneum and Kallikrein-related peptidase (KLK) 7 in the stratum corneum and protease activated receptor (PAR)-2 were observed to confirm the inhibition of the inflammation, Phosphorylated extracellular signal-related kinase (p-ERK), Phosphorylated mammalian target of rapamycin (p-mTOR), and E-Cadherin were observed to confirm microenvironmental regulation. Results: β-GT was significantly increased in CB1, CB2, and GPR55 positive reactions compared to that of the ADE. In positive reaction of the filaggrin in the stratum corneum, β-GT was significantly increased than that of the ADE. For KLK7 positive and PAR2 positive, β-GT was significantly reduced compared to the ADE. The p-ERK-positive and p-mTOR-positive reactions were significantly reduced in β-GT than in ADE. E-cadherin positive reaction was significantly increased in β-GT than in ADE (All p < 0.01). Conclusions: It was confirmed that β-glucan has the effect of inhibiting the epithelium induced by atopic dermatitis through the ECS activity.

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