Oat β-glucan repairs the epidermal barrier by upregulating the levels of epidermal differentiation, cell-cell junctions and lipids via Dectin-1

燕麦β-葡聚糖通过 Dectin-1 上调表皮分化、细胞间连接和脂质水平,修复表皮屏障

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作者:Rongrong Jing, Mengli Fu, Yuhan Huang, Kaini Zhang, Jiabin Ye, Fanghua Gong, Al-Bashari Jihea Ali Naji Nasser, Xiashun Xu, Jiali Xiao, Guangdong Yu, Shisheng Lin, Wengang Zhao, Nuo Xu, Xiaokun Li, Zhiming Li, Shuang Gao

Background and purpose

Oat β-glucan could ameliorate epidermal hyperplasia and accelerate epidermal barrier repair. Dectin-1 is one of the receptors of β-glucan and many biological functions of β-glucan are mediated by Dectin-1. Dectin-1 promotes wound healing through regulating the proliferation and migration of skin cells. Thus, this study aimed to investigate the role of oat β-glucan and Dectin-1 in epidermal barrier repair. Experimental approach: To investigate the role of Dectin-1 in the epidermal barrier, indicators associated with the recovery of a damaged epidermal barrier, including histopathological changes, keratinization, proliferation, apoptosis, differentiation, cell-cell junctions and lipid content were compared between WT and Dectin-1-/- mice. Further, the effect of oat β-glucan on the disruption of the epidermal barrier was also compared between WT and Dectin-1-/- mice. Key

Purpose

Oat β-glucan could ameliorate epidermal hyperplasia and accelerate epidermal barrier repair. Dectin-1 is one of the receptors of β-glucan and many biological functions of β-glucan are mediated by Dectin-1. Dectin-1 promotes wound healing through regulating the proliferation and migration of skin cells. Thus, this study aimed to investigate the role of oat β-glucan and Dectin-1 in epidermal barrier repair. Experimental approach: To investigate the role of Dectin-1 in the epidermal barrier, indicators associated with the recovery of a damaged epidermal barrier, including histopathological changes, keratinization, proliferation, apoptosis, differentiation, cell-cell junctions and lipid content were compared between WT and Dectin-1-/- mice. Further, the effect of oat β-glucan on the disruption of the epidermal barrier was also compared between WT and Dectin-1-/- mice. Key

Results

Dectin-1 deficiency resulted in delayed recovery and marked keratinization, as well as abnormal levels of keratinocyte differentiation, cell-cell junctions and lipid synthesis during the restoration of the epidermal barrier. Oat β-glucan significantly reduces epidermal hyperplasia, promotes epidermal differentiation, increases cell-cell junction expression, promotes lipid synthesis and ultimately accelerates the recovery of damaged epidermal barriers via Dectin-1. Oat β-glucan could promote CaS receptor expression and activate the PPAR-γ signalling pathway via Dectin-1.

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