Irisin alleviates lung injury in asthma mice by inhibiting phosphoinositide-3-kinase-protein kinase B (PI3K/AKT) phosphorylation and release of inflammatory factors

Abstract

Asthma refers to a common chronic airway inflammation disease, which is accompanied by T type 2 (Th2) mediated reaction and inflammatory factor excessive expression. The relationship between irisin and asthmatic lung injury is poorly reported. Employed ovalbumin (OVA) treatment was used to induce asthma rat model, and rats were then treated with irisin or PI3K/AKT pathway inhibitors. The reactivity of rats after different treatments was observed by immunohistochemical analysis of lung tissue damage degree and enzyme-linked immunosorbent assay (ELISA), to detect serum and release of inflammatory factors in lung and bronchial lavage fluid. Protein phosphorylation was observed by Western blot analysis of PI3K/AKT pathway activation. Irisin improved the general condition of asthmatic model rats and reduced damage to lung tissue. In addition, irisin significantly reduced PI3K/AKT phosphorylation, which was induced by OVA and suppressed inflammation factors level in bronchoalveolar lavage fluid and serum. Beneficial effect of irisin in reducing the levels of inflammatory factors in serum and BALF of rats was similar to that of PI3K/AKT pathway inhibitors. Irisin effectively reduced the OVA induced asthma model rats with lung injury, with inhibition of PI3K/AKT pathway phosphorylation and inflammatory related cytokines release. Results from this study not only shows irisin is an effective active molecules to treat asthma, but at the same time suppresses phosphorylation of PI3K/AKT axis in the progress of asthma and inflammation factors, and the specificity of the PI3K/AKT pathway inhibitor may also be potential targets for asthma treatment.