Yu Cheng-Xiu, Shi Zu-An, Ou Guo-Chun, Chen Xiao-Ju, Liu Qin, Zeng Di, Nie Xue-Ju, Chen Jian-Jun
Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, China.
Department of Anesthesiology, Nanchong Central Hospital, The Second Clinical College of North Sichuan Medical College, Nanchong, Sichuan 637000, China.
Mol Immunol. 2022 Jun;146:78-86. doi: 10.1016/j.molimm.2022.03.118. Epub 2022 Apr 21.
Asthma is a chronic inflammatory disease of the respiratory system. Maresin-2 (MaR2) is biosynthesized from docosahexaenoic acid (DHA) by macrophages, display strong anti-inflammatory and pro-resolving activity. To investigate the therapeutic effect and mechanism of MaR2 on asthmatic mice induced by ovalbumin (OVA) in conjunction with the adjuvant aluminum hydroxide. Twenty four female BALB/c mice were randomly divided into control, OVA, OVA + MaR2, and OVA + dexamethasone (Dexa) groups. MaR2 or Dexa were given as a treatment for OVA-induced asthma. Serum, bronchoalveolar alveolar lavage fluid (BALF) and lung tissue were collected for further analysis. The Pathological changes of lung tissue, proportion of inflammatory cells in BALF, levels of inflammatory cytokines in BALF or serum, oxidative stress indices, and the protein concentration of ASC, MPO, Ly-6G, ICAM-1, NLRP3 and Caspase-1 in lung tissues were evaluated. Compared with the OVA group, both OVA + MaR2 and OVA + Dexa group had reduced inflammation and mucus secretion in lung tissue, number of inflammatory cells in BALF, levels of related inflammatory cytokines in serum or BALF, and expressions of ASC, MPO, Ly-6G, ICAM-1, NLRP3 and Caspase-1 proteins in lung tissue. In addition, the oxidative stress was alleviated as indicated by decreased MDA, and elevated SOD and GSH. MaR2 has an obvious protective effect on OVA-induced bronchial asthma in mice, in a similar manner as Dexa. The mechanism may be related to the inhibition of the Th2 type immune response, the NLRP3 inflammasome activation and oxidative stress.
哮喘是一种呼吸系统的慢性炎症性疾病。maresin-2（MaR2）由巨噬细胞从二十二碳六烯酸（DHA）生物合成，具有强大的抗炎和促炎症消退活性。为了研究MaR2对卵清蛋白（OVA）联合佐剂氢氧化铝诱导的哮喘小鼠的治疗效果及机制。将24只雌性BALB/c小鼠随机分为对照组、OVA组、OVA + MaR2组和OVA + 地塞米松（Dexa）组。给予MaR2或Dexa治疗OVA诱导的哮喘。收集血清、支气管肺泡灌洗液（BALF）和肺组织进行进一步分析。评估肺组织的病理变化、BALF中炎症细胞比例、BALF或血清中炎症细胞因子水平、氧化应激指标以及肺组织中ASC、MPO、Ly-6G、ICAM-1、NLRP3和Caspase-1的蛋白浓度。与OVA组相比，OVA + MaR2组和OVA + Dexa组肺组织中的炎症和黏液分泌均减少，BALF中炎症细胞数量、血清或BALF中相关炎症细胞因子水平以及肺组织中ASC、MPO、Ly-6G、ICAM-1、NLRP3和Caspase-1蛋白的表达均降低。此外，氧化应激得到缓解，表现为MDA降低，SOD和GSH升高。MaR2对OVA诱导的小鼠支气管哮喘具有明显的保护作用，其作用方式与Dexa相似。其机制可能与抑制Th2型免疫反应、NLRP3炎性小体激活和氧化应激有关。
