Abbas Alaa Hamza, Abbood Muayad Sraibet, Ridha-Salman Hayder, Fakhri Salar Ayad, Abbas Zahraa Hamza, Al-Athari Ali Jihad Hemid
Department of Pharmacology, College of Pharmacy, Al-Mustaqbal University, 51001, Hillah, Babylon, Iraq.
Department of Applied Embryology, High Institute for Infertility Diagnosis and Assisted Reproductive Technologies, Al-Nahrain University, Baghdad, Iraq.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jun 3. doi: 10.1007/s00210-025-04317-2.
Psoriasis is a chronic inflammatory skin disorder that is triggered by immune-mediated, genetic, and environmental factors. Moxifloxacin is a fluoroquinolone antibiotic with extended non-expected anti-inflammatory and immune-modulating effects. This study aims to investigate the possible influence of two different concentrations of moxifloxacin emulgel on psoriasis induced via imiquimod in mice. Dividing 48 mice into six groups (8 mice for each group), all groups gated imiquimod to induce psoriasis (except group I) for 7 days. The induction group (Group II) received imiquimod cream for 7 days. The vehicle group obtained emulgel base for 7 days. The rest of the groups got calcipotriol 0.005% ointment, moxifloxacin 3% emulgel, and moxifloxacin 5% emulgel, respectively, once daily for a further 7 days after the induction period. Topical moxifloxacin had important anti-psoriatic activity by diminishing the Psoriasis Area Severity Index (PASI) scores and improving histological alterations during imiquimod application. Moreover, moxifloxacin significantly lowered the levels of inflammatory biomarkers like TGF-β, TNF-α, IL-17, IL-1β, IL-23, and VEFG while increasing levels of anti-inflammatory biomarkers IL-10 and IL-37. Moxifloxacin also suppressed oxidative indicators such as MDA and elevated antioxidant enzyme levels, such as catalase. Moxifloxacin has substantial anti-psoriatic action against imiquimod-induced psoriasis through its anti-proliferative and anti-inflammatory effects. Furthermore, moxifloxacin has a restorative effect on the histopathological alterations of mice's skin induced by imiquimod.
银屑病是一种由免疫介导、遗传和环境因素引发的慢性炎症性皮肤病。莫西沙星是一种氟喹诺酮类抗生素，具有意外的抗炎和免疫调节作用。本研究旨在探讨两种不同浓度的莫西沙星乳胶对咪喹莫特诱导的小鼠银屑病的可能影响。将48只小鼠分为六组（每组8只），除第一组外，所有组均用咪喹莫特诱导银屑病7天。诱导组（第二组）接受咪喹莫特乳膏治疗7天。赋形剂组接受乳胶基质治疗7天。其余各组在诱导期后，分别每天一次给予0.005%卡泊三醇软膏、3%莫西沙星乳胶和5%莫西沙星乳胶，持续7天。局部应用莫西沙星通过降低银屑病面积严重程度指数（PASI）评分和改善咪喹莫特应用期间的组织学改变，具有重要的抗银屑病活性。此外，莫西沙星显著降低了TGF-β、TNF-α、IL-17、IL-1β、IL-23和VEFG等炎症生物标志物的水平，同时提高了抗炎生物标志物IL-10和IL-37的水平。莫西沙星还抑制了MDA等氧化指标，并提高了过氧化氢酶等抗氧化酶水平。莫西沙星通过其抗增殖和抗炎作用，对咪喹莫特诱导的银屑病具有显著的抗银屑病作用。此外，莫西沙星对咪喹莫特诱导的小鼠皮肤组织病理学改变具有修复作用。
