Morin attenuates cigarette smoke-induced lung inflammation through inhibition of PI3K/AKT/NF-κB signaling pathway.

Abstract Cigarette smoke (CS) is a major factor that leads to lung inflammation. The prevalence of CS-induced lung injury has continuously increased worldwide. Morin exists in a large member of plants and fruits that has been reported to have antioxidant and anti-inflammatory properties. In the present study, we tested the mechanism and protective effects of morin on CS-induced lung inflammation in mice. The mice were exposed to CS for 2 h twice a day for 4 weeks. Morin (10, 20, and 40 mg/kg) was treated to mice through oral gavage 1 h before CS administration. 24 h after the last CS exposure, the mice were euthanized. The lung tissues were collected and the pathological changes, wet/dry ratio, MPO activity, MDA levels, and P13K/ATK/NF-κB signaling pathway expression were detected. The bronchial alveolar lavage fluid (BALF) was obtained and the levels of inflammatory cells and inflammatory cytokines were measured. The results showed that morin treatment significantly inhibited lung pathological changes, wet/dry ratio, MPO activity, and MDA level. The levels of total cells, neutrophils, macrophages, as well as the production of inflammatory cytokines in the BALF induced by CS were also suppressed by morin. Further research showed that morin dramatically suppressed the activation of P13K/ATK/NF-κB singling pathway induced by CS. This study highlights the protective effects of morin on CS-induced lung inflammation, which may, at least part, be mediated through inhibiting P13K/ATK/NF-κB signaling pathway. These finding demonstrated that morin could be a potential drug for CS-induced lung injury. Highlights • Morin inhibited the pathological changes, wet/dry ratio, MPO activity, and MDA levels of lung tissues. • Morin suppressed the levels of total cells, neutrophils, macrophages, as well as the production of inflammatory cytokines. • Morin dramatically suppressed the activation of P13K/ATK/NF-κB singling pathway induced by CS. [ABSTRACT FROM AUTHOR]