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燕麦 β-葡聚糖通过 dectin-1 介导的 ERK 和 p38 信号通路上调 CaSR 的表达来改善表皮屏障破坏。

Oat β-glucan ameliorates epidermal barrier disruption by upregulating the expression of CaSR through dectin-1-mediated ERK and p38 signaling pathways.

机构信息

College of Life and Environmental Sciences, Wenzhou University, Wenzhou 325035, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.

College of Life and Environmental Sciences, Wenzhou University, Wenzhou 325035, China.

出版信息

Int J Biol Macromol. 2021 Aug 31;185:876-889. doi: 10.1016/j.ijbiomac.2021.07.002. Epub 2021 Jul 5.

DOI:10.1016/j.ijbiomac.2021.07.002
PMID:34237364
Abstract

The integrity of the epidermal barrier and the maintenance of barrier homeostasis depend on the dynamic balance between the proliferation and differentiation of keratinocytes. Calcium (Ca) plays a crucial role in maintaining a balance of these two processes as well as in the formation of an epidermal permeability barrier. In this study, we showed that topical application of oat β-glucan (OG) could ameliorate epidermal hyperplasia and accelerate the recovery of the epidermal barrier by promoting epidermal differentiation. Mechanistic studies revealed a positive interaction between OG and the dectin-1 receptor, and this interaction could lead to an upregulated expression of the calcium-sensing receptor (CaSR) via activation of the downstream ERK and p38 pathways. This consequently increased the sensitivity of keratinocytes to extracellular Ca under the condition of calcium loss following the disruption of the epidermal barrier, resulting in the maintenance of normal keratinocyte differentiation in the epidermis, and ultimately promoting the recovery of the epidermal barrier. These findings clearly demonstrated the healing effect of OG on a physically damaged epidermal barrier. Thus, OG could be considered a valuable component in the development of skin repair agents.

摘要

表皮屏障的完整性和屏障稳态的维持依赖于角质形成细胞的增殖和分化之间的动态平衡。钙(Ca)在维持这两个过程的平衡以及形成表皮渗透性屏障方面起着至关重要的作用。在这项研究中,我们表明,燕麦β-葡聚糖(OG)的局部应用可以通过促进表皮分化来改善表皮过度增生并加速表皮屏障的恢复。机制研究表明,OG 与 dectin-1 受体之间存在积极的相互作用,这种相互作用可以通过激活下游的 ERK 和 p38 途径来上调钙敏感受体(CaSR)的表达。这继而增加了角质形成细胞在表皮屏障破坏后细胞外 Ca 丢失情况下对细胞外 Ca 的敏感性,导致表皮中正常角质形成细胞分化的维持,并最终促进表皮屏障的恢复。这些发现清楚地表明了 OG 对物理损伤的表皮屏障的愈合作用。因此,OG 可以被认为是开发皮肤修复剂的有价值的成分。

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