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

Abstract 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 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. Conclusion and Implications Oat β ‐glucan promote the recovery of damaged epidermal barriers through promoting epidermal differentiation, increasing the expression of cell–cell junctions and lipid synthesis through Dectin‐1. Dectin‐1 deficiency delay the recovery of epidermal barriers, which indicated that Dectin‐1 may be a potential target in epidermal barrier repair.