Ardizzone Alessio, Repici Alberto, Capra Anna Paola, De Gaetano Federica, Bova Valentina, Casili Giovanna, Campolo Michela, Esposito Emanuela
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno d'Alcontres, 98166 Messina, Italy.
Antioxidants (Basel). 2023 Jun 15;12(6):1278. doi: 10.3390/antiox12061278.
Atopic dermatitis (AD) is the most common chronically relapsing inflammatory skin disease, predominantly common in children; it is characterized by an eczematous pattern generally referable to skin dryness and itchy papules that become excoriated and lichenified in the more advanced stages of the disease. Although the pathophysiology of AD is not completely understood, numerous studies have demonstrated the complex interaction between genetic, immunological, and environmental factors, which acts to disrupt skin barrier function. Free radicals play a key role by directly damaging skin structure, inducing inflammation and weakening of the skin barrier. Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl) is a membrane-permeable radical scavenger, known to be a stable nitroxide, which exhibits excellent antioxidant effects in several human disorders, such as osteoarthritis and inflammatory bowel diseases. Considering the few existing studies on dermatological pathologies, this study aimed to evaluate tempol, in a cream formulation, in a murine model of AD. Dermatitis was induced in mice via dorsal skin application of 0.5% Oxazolone, three times a week for two weeks. After induction, mice were treated with tempol-based cream for another two weeks at three different doses of 0.5%, 1% and 2%. Our results demonstrated the ability of tempol, at the highest percentages, to counteract AD by reducing the histological damage, decreasing mast cell infiltration, and improving the skin barrier properties, by restoring the tight junction (TJs) and filaggrin. Moreover, tempol, at 1% and 2%, was able to modulate inflammation by reducing the nuclear factor kappa-light-chain-enhancer of the activated B cell (NF-κB) pathway, as well as tumor necrosis factor (TNF)-α and interleukin (IL)-1β expression. Topical treatment also attenuated oxidative stress by modulating nuclear factor erythroid 2-related factor 2 (Nrf2), manganese superoxide dismutase (MnSOD), and heme oxygenase I (HO-1) expression levels. The obtained results demonstrate the numerous advantages provided by the topical administration of a tempol-based cream formulation, in reducing inflammation and oxidative stress through modulation of the NF-κB/Nrf2 signaling pathways. Therefore, tempol could represent an alternative anti-atopic approach to treating AD, thereby improving skin barrier function.
特应性皮炎(AD)是最常见的慢性复发性炎症性皮肤病,主要多见于儿童;其特征为湿疹样皮疹,通常与皮肤干燥和瘙痒性丘疹有关,在疾病的更晚期会出现糜烂和苔藓化。尽管AD的病理生理学尚未完全了解,但大量研究表明遗传、免疫和环境因素之间存在复杂的相互作用,这种相互作用会破坏皮肤屏障功能。自由基通过直接损伤皮肤结构、引发炎症和削弱皮肤屏障而发挥关键作用。Tempol(4-羟基-2,2,6,6-四甲基哌啶-1-氧基)是一种可透过细胞膜的自由基清除剂,已知是一种稳定的氮氧化物,在骨关节炎和炎症性肠病等多种人类疾病中表现出优异的抗氧化作用。考虑到现有关于皮肤病学病理学的研究较少,本研究旨在评估乳膏制剂形式的Tempol在AD小鼠模型中的作用。通过每周三次在小鼠背部皮肤涂抹0.5%的恶唑酮,持续两周来诱导皮炎。诱导后,用三种不同剂量(0.5%、1%和2%)的基于Tempol的乳膏对小鼠再治疗两周。我们的结果表明,最高百分比的Tempol能够通过减少组织学损伤、减少肥大细胞浸润以及通过恢复紧密连接(TJs)和丝聚蛋白来改善皮肤屏障特性,从而对抗AD。此外,1%和2%的Tempol能够通过减少活化B细胞的核因子κB轻链增强子(NF-κB)途径以及肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β的表达来调节炎症。局部治疗还通过调节核因子红细胞2相关因子2(Nrf2)、锰超氧化物歧化酶(MnSOD)和血红素加氧酶I(HO-1)的表达水平来减轻氧化应激。所得结果表明,基于Tempol的乳膏制剂局部给药通过调节NF-κB/Nrf2信号通路在减轻炎症和氧化应激方面具有诸多优势。因此,Tempol可能代表一种治疗AD的替代抗特应性方法,从而改善皮肤屏障功能。