Autophagy-mediated regulation of psoriasis biomarkers by Dead Sea and magnetized saline waters: An in vitro study.

Neuro endocrinology letters Pub Date : 2025-04-28
Piercarlo Minoretti, Enzo Emanuele, Celia García-Chico, Kayvan Khoramipour, Alejandro Santos-Lozano, Eugenia V Di Brizzi, Simone Lista
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Abstract

Background: Dysregulated autophagy is linked to abnormal keratinocyte differentiation and persistent psoriatic inflammation. Smart fluids, such as Dead Sea Water (DSW) and saline magnetized water (MW), have emerged as potential non-pharmacological autophagy activators. This study evaluates their effects on psoriasis-like keratinocytes, focusing on calcitonin gene-related peptide (CGRP), a neuropeptide involved in pruritus and inflammation, and secreted frizzled-related protein 4 (SFRP4), whose reduced expression contributes to epidermal hyperplasia. The role of autophagy in mediating these effects was also investigated.

Methods: Polycytokine-stimulated HaCaT keratinocytes were treated with DSW or saline MW. CGRP and SFRP4 expression levels were assessed alongside autophagy markers beclin-1 and LC3B. The involvement of autophagy was confirmed using wortmannin, an autophagy inhibitor.

Results: Both DSW (4.7 ± 1.9 a.u.) and saline MW (3.6 ± 1.6 a.u.) significantly reduced CGRP expression compared to controls (non-magnetized saline: 7.5 ± 2.3 a.u.; distilled water: 7.6 ± 2.5 a.u.; all p< 0.001). While both fluids enhanced SFRP4 expression equally (p = 0.78), saline MW showed superior CGRP inhibition (p< 0.001). Both fluids mitigated polycytokine-induced reductions in beclin-1 and LC3B levels (all p< 0.001), with saline MW showing more pronounced effects (p< 0.05). Wortmannin impaired the effects of both fluids on CGRP and SFRP4, indicating autophagy mediation.

Conclusions: DSW and saline MW show promise as sustainable active ingredients for topical formulations targeting psoriatic inflammation via autophagy activation.

死海和磁化盐水对牛皮癣生物标志物自噬介导的调节:一项体外研究
背景:失调的自噬与角质细胞异常分化和持续的银屑病炎症有关。智能流体,如死海水(DSW)和盐水磁化水(MW),已经成为潜在的非药物自噬激活剂。本研究评估了它们对牛皮癣样角质形成细胞的影响,重点关注降钙素基因相关肽(CGRP),一种与瘙痒和炎症有关的神经肽,以及分泌卷曲相关蛋白4 (SFRP4),其表达减少有助于表皮增生。自噬在介导这些作用中的作用也被研究。方法:多细胞因子刺激的HaCaT角质形成细胞用DSW或生理盐水处理。检测CGRP和SFRP4与自噬标志物beclin-1和LC3B的表达水平。使用自噬抑制剂wortmannin证实了自噬的参与。结果:与对照组相比,DSW(4.7±1.9 a.u)和生理盐水MW(3.6±1.6 a.u)均显著降低CGRP表达(未磁化生理盐水:7.5±2.3 a.u;蒸馏水:7.6±2.5 a.u.;均p< 0.001)。两种液体均增强了SFRP4的表达(p = 0.78),盐水MW表现出更好的CGRP抑制(p< 0.001)。两种液体都减轻了多细胞因子引起的beclin-1和LC3B水平的降低(均p< 0.001),盐水MW表现出更明显的效果(p< 0.05)。Wortmannin破坏了两种液体对CGRP和SFRP4的影响,表明自噬介导。结论:DSW和生理盐水MW有望通过自噬激活作为局部配方靶向银屑病炎症的可持续活性成分。
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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