Protective Effects of Recombined Mussel Adhesive Protein against AD Skin Inflammation in Mice

IF 3.4 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yu Wu, Feng Li, Yan Gong, Xing Wan, Liming Zhou
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Abstract

(1) Background: Atopic dermatitis (AD) is characterized as a chronic inflammatory skin disease with a significant incidence rate. The pathophysiological mechanisms underlying AD remain incompletely understood. However, extensive research demonstrates that a complex interplay among genetic, immune, and environmental factors contributes to the disruption of skin barrier function. Inflammation is identified as one of the pathological mechanisms in AD. Recombined mussel adhesive protein exhibits anti-inflammatory properties. However, recombinant mussel adhesive protein has been used less frequently for AD, so we explored the therapeutic effect of recombinant mussel adhesive protein for AD and the potential mechanism. (2) Methods: We established a mice model of AD in vivo and an LPS-induced inflammation model in HaCaT cells in vitro. Through assessment of skin lesion scores, itch frequency, transepidermal water loss, skin microcirculation, HE staining, Elisa assays for IL-6, IL-12, IL-13, IL-4, IL-5, IFN-γ, IgE, and TNF-α, immunohistochemical staining for filaggrin and CK14, Masson staining, and Western blot analysis of NF-κB p65, P-P65, Keap1, and Nrf2, the effects of recombined mussel adhesive protein on AD symptoms, pathology, inflammation, and its mechanisms are investigated. (3) Results: The recombined mussel adhesive protein significantly improved the compromised skin barrier, reduced scratching frequency in mice, decreased transepidermal water loss, and lowered the expression of inflammatory factors, thus ameliorating skin inflammation damage. Mechanistically, recombined mussel adhesive protein downregulated the expression of P-p65/p65 and Keap1 while upregulating the level of Nrf2. (4) Conclusions: Overall, our results demonstrate the effectiveness of recombined mussel adhesive protein in attenuating DNFB-induced AD by inhibiting NF-κB and activating the Keap1/Nrf2 signaling pathway. Thus, recombined mussel adhesive protein is a promising therapeutic candidate for the treatment of AD.
重组贻贝粘合蛋白对小鼠 AD 皮肤炎症的保护作用
(1) 背景:特应性皮炎(AD)是一种慢性炎症性皮肤病,发病率很高。特应性皮炎的病理生理机制仍不完全清楚。然而,大量研究表明,遗传、免疫和环境因素之间复杂的相互作用导致了皮肤屏障功能的破坏。炎症被认为是注意力缺失症的病理机制之一。重组贻贝粘合蛋白具有抗炎特性。因此,我们探讨了重组贻贝粘合蛋白对AD的治疗效果及其潜在机制。(2)方法:我们在体内建立了 AD 小鼠模型,在体外建立了 LPS 诱导的 HaCaT 细胞炎症模型。通过评估皮损评分、瘙痒频率、经表皮失水、皮肤微循环、HE 染色、IL-6、IL-12、IL-13、IL-4、IL-5、IFN-γ、IgE 和 TNF-α 的 Elisa 检测、filaggrin 和 CK14 的免疫组化染色、Masson 染色和 Western bl bl、Masson染色,以及NF-κB p65、P-P65、Keap1和Nrf2的Western印迹分析,研究重组贻贝粘合蛋白对AD症状、病理、炎症及其机制的影响。(3)结果:重组贻贝粘合蛋白能明显改善受损的皮肤屏障,降低小鼠搔抓频率,减少经表皮失水,降低炎症因子的表达,从而改善皮肤炎症损伤。从机理上讲,重组贻贝粘合蛋白下调了 P-p65/p65 和 Keap1 的表达,同时上调了 Nrf2 的水平。(4)结论:总之,我们的研究结果表明,重组贻贝粘附蛋白通过抑制NF-κB和激活Keap1/Nrf2信号通路,有效地减轻了DNFB诱导的AD。因此,重组贻贝粘合蛋白是一种治疗AD的有希望的候选疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cosmetics
Cosmetics Medicine-Surgery
CiteScore
5.20
自引率
12.10%
发文量
108
审稿时长
8 weeks
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