卡格列净对咪喹莫特诱导的银屑病样炎症小鼠模型的缓解作用

Hayder Ridha-Salman, Adeeb Ahmed Al-Zubaidy, Alaa Hamza Abbas, Dhuha M Hassan, Samir A Malik
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引用次数: 0

摘要

银屑病是一种免疫介导的终身性皮肤病,皮肤会出现增厚、发红和脱屑的斑块。卡格列净是一种格列酮类抗糖尿病药物,具有非典型的显著抗氧化、抗炎、抗增殖和免疫调节作用。本研究旨在探讨局部卡格列净对咪喹莫特诱发的银屑病样皮炎小鼠模型的可能影响。本研究评估了 20 只瑞士白小鼠,将其随机分为 4 组,每组 5 只。除对照组外,每只小鼠都在剃光的背部局部涂抹咪喹莫特,持续 7 天。对照组包括未接受任何治疗的健康小鼠。其他三组小鼠在使用咪喹莫特乳膏的同一天分别接受了载体(诱导组)、0.05% 丙酸氯倍他索软膏(氯倍他索组)或 4% 卡格列净凝胶(卡格列净 4% 组)的局部治疗。外用卡格列净明显降低了咪喹莫特诱发的银屑病疹的强度,包括发红、亮白色鳞屑和棘层增生,同时还纠正了组织病理学畸变。给暴露于咪喹莫特的动物服用卡那格列净可显著降低皮肤炎症介质的浓度,如IL-8、IL-17、IL-23和TNF-α,同时提高IL-10的水平。卡格列净还进一步降低了涉及 Ki-67 和 PCNA 的增殖因子,减少了 MDA 和 MPO 等氧化指标,并增强了抗氧化指标的活性,尤其是 SOD 和 CAT。Canagliflozin可以缓解咪喹莫特诱导的银屑病动物模型,这可能得益于它的抗炎、抗氧化、抗血管生成和抗增殖活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The alleviative effects of canagliflozin on imiquimod-induced mouse model of psoriasis-like inflammation

The alleviative effects of canagliflozin on imiquimod-induced mouse model of psoriasis-like inflammation

Psoriasis is a life-long immune-mediated dermatosis with thickened, reddish, and flaky skin patches. Canagliflozin is a gliflozin antidiabetic with non-classical remarkable antioxidative, anti-inflammatory, anti-proliferative, and immune-modulating effects. The aim of this study is to examine the probable effects of topical canagliflozin on a mouse model of imiquimod-provoked psoriasis-like dermatitis. The study evaluated 20 Swiss white mice, sorted haphazardly into 4 groups of 5 animals each. Every mouse, with the exception of the control group, had imiquimod applied topically to their shaved backs for 7 days. The control group included healthy mice that were not given any treatment. Mice in the other three groups underwent topical treatment with vehicle (induction group), 0.05% clobetasol propionate ointment (clobetasol group), or 4% canagliflozin emulgel (canagliflozin 4% group) on exactly the same day as imiquimod cream was administered. Topical canagliflozin markedly lowered the intensity of imiquimod-provoked psoriasis eruptions, featuring redness, glossy-white scales, and acanthosis, while also correcting histopathological aberrations. Canagliflozin administration to imiquimod-exposed animals resulted in significantly decreased cutaneous concentrations of inflammatory mediators such as IL-8, IL-17, IL-23, and TNF-α, with raised levels of IL-10. Canagliflozin further lowered proliferative factors involving Ki-67 and PCNA, diminished oxidative indicators such as MDA and MPO, and augmented the activity of antioxidant markers, notably SOD and CAT. Canagliflozin might alleviate the imiquimod-induced animal model of psoriasis, probably thanks to its profound anti-inflammatory, antioxidant, antiangiogenic, and antiproliferative activities.

Graphic Abstract

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