TY - JOUR A2 - Cervellati, Carlo AU - Ou, Guochun AU - Liu, Qin AU - Yu, Chengxiu AU - Chen, Xiaoju AU - Zhang, Wenbo AU - Chen, Yong AU - Wang, Tao AU - Luo, Yongqiang AU - Jiang, Guolu AU - Zhu, Mingmei AU - Li, Hongmei AU - Zeng, Mei PY - 2021 DA - 2021/02/10 TI - The Protective Effects of Maresin 1 in the OVA-Induced Asthma Mouse Model SP - 4131420 VL - 2021 AB - Asthma is a chronic inflammatory disease that cannot be cured. Maresin 1 (MaR1) is a specific lipid synthesized by macrophages that exhibits powerful anti-inflammatory effects in various inflammatory diseases. The goal of this study was to evaluate the effect of MaR1 on allergic asthma using an ovalbumin- (OVA-) induced asthma model. Thirty BALB/c mice were randomly allocated to control, OVA, and MaR1 + OVA groups. Mice were sacrificed 24 hours after the end of the last challenge, and serum, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for further analysis. Western blotting was used to measure the protein level of IκBα, the activation of the NF-κB signaling pathway, and the expression of NF-κB downstream inflammatory cytokines. Quantitative real-time polymerase chain reactions (qRT-PCRs) were used to evaluate the expression levels of COX-2 and ICAM-1 in lung tissues. We found that high doses of MaR1 were most effective in preventing OVA-induced inflammatory cell infiltration and excessive mucus production in lung tissue, reducing the number of inflammatory cells in the BALF and inhibiting the expression of serum or BALF-associated inflammatory factors. Furthermore, high-dose MaR1 treatment markedly suppressed the activation of the NF-κB signaling pathway, the degradation of IκBα, and the expression of inflammatory genes downstream of NF-κB, such as COX-2 and ICAM-1, in the OVA-induced asthma mouse model. Our findings indicate that MaR1 may play a critical role in OVA-induced asthma and may be therapeutically useful for the management of asthma. SN - 0962-9351 UR - https://doi.org/10.1155/2021/4131420 DO - 10.1155/2021/4131420 JF - Mediators of Inflammation PB - Hindawi KW - ER -