Pretreatment with acetylsalicylic acid alleviates UVB irradiation-induced skin pathology in hairless mice and BOC-2 (an ALX/FPR2 receptor antagonist) reduces its activity

Renata M. Martinez , Priscila Saito , Ingrid C. Pinto , Camilla C.A. Rodrigues , Victor Fattori , Cristina P.B. Melo , Allan J.C. Bussmann , Larissa Staurengo-Ferrari , Tiago H. Zaninelli , Telma Saraiva-Santos , Michel F. Otuki , Daniela A. Cabrini , Marcela M. Baracat , Sandra R. Georgetti , Waldiceu A. Verri Jr. , Rubia Casagrande
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Abstract

This work aims to investigate if the biological activity of acetylsalicylic acid (ASA) against UVB irradiation-induced skin inflammatory and oxidative injury in hairless mice would be amenable by treatment with BOC-2, an antagonist of the formyl peptide receptor 2 receptor (ALX/FPR2). Mice were treated with BOC-2 and after 30 minutes, they received ASA or Aspirin-Triggered 15-epi-lipoxin A4 (AT-LXA4, an agonist of ALX/FPR2), and after 1 hour, they were exposed to UVB irradiation (dose of 4.14 J/cm2). UVB stimulation induced neutrophil and mast cell recruitment, edema, matrix metalloproteinase-9 (MMP-9) activity, collagen degradation, sunburn cell formation, and cytokine production (TNF-α, IL-1β and IL-6). All these parameters were inhibited by ASA or AT-LXA4. In addition, ASA and AT-LXA4 enhanced anti-inflammatory cytokines (IL-10 and TGF-β), and attenuated UVB-induced oxidative damage returning the oxidative status to baseline levels in parameters such as ferric reducing ability, free radical scavenging, reduced glutathione levels, catalase activity, superoxide anion production, Nrf2, Nqo1, and gp91phox mRNA expression. These therapeutic effects of ASA and AT-LXA4 were reversed by BOC-2. Our results demonstrate that ALX/FPR2 receptor plays an important role in ASA activity against UVB-induced skin pathologies.
乙酰水杨酸预处理可减轻UVB照射引起的无毛小鼠皮肤病理,而bac -2(一种ALX/FPR2受体拮抗剂)可降低其活性
本研究旨在探讨乙酰水杨酸(ASA)对UVB照射引起的无毛小鼠皮肤炎症和氧化损伤的生物活性是否可以通过甲酰基肽受体2受体(ALX/FPR2)拮抗剂BOC-2处理。用BOC-2处理小鼠,30 分钟后,给予ASA或阿斯匹林触发的15-肾上腺素脂素A4 (AT-LXA4, ALX/FPR2的激动剂),1 小时后,暴露于UVB照射(剂量为4.14 J/cm2)。UVB刺激诱导中性粒细胞和肥大细胞募集、水肿、基质金属蛋白酶-9 (MMP-9)活性、胶原降解、晒伤细胞形成和细胞因子(TNF-α、IL-1β和IL-6)的产生。ASA或AT-LXA4均对上述指标有抑制作用。此外,ASA和AT-LXA4增强抗炎细胞因子(IL-10和TGF-β),并减弱uva诱导的氧化损伤,使氧化状态在铁还原能力、自由基清除能力、还原型谷胱甘肽水平、过氧化氢酶活性、超氧阴离子产生、Nrf2、Nqo1和gp91phox mRNA表达等参数中恢复到基线水平。ASA和AT-LXA4的这些治疗作用被BOC-2逆转。我们的研究结果表明,ALX/FPR2受体在ASA对抗uvb诱导的皮肤病变的活性中起重要作用。
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