Genkwanin improves inflammatory injury in rats with septic lung injury by regulating NF-κB signaling pathway

Abstract

To assess possible effects of genkwanin (GKA) in septic lung injury and its related mechanisms. An animal model of cecal ligation and puncture (CLP)-induced acute lung injury was constructed. Histological analysis and wet–dry (W/D) ratio of the lung tissue were observed. The cell apoptosis in this model was analyzed by caspase activity detection, protein levels of B-cell lymphoma protein 2 (Bcl-2) and Bcl-2-associated X (Bax), and cell inflammation in CLP model; after GKA treatment, it was analyzed by enzyme-linked-immunosorbent serologic assay (ELISA). The involvement of nuclear factor kappa B (NF-κB) signaling pathway was evaluated by Immunoblot assay. We constructed an animal model of CLP-induced acute lung injury. Our data revealed that GKA reduced lung edema and inflammation in CLP mice. In addition, GKA reduced lung injury and apoptosis in CLP mice. Mechanically, our data in addition confirmed that GKA improved inflammatory injury in CLP mice by regulating NF-κB signaling pathway. Our data therefore confirmed that GKA could serve as a promising drug for the treatment of sepsis-induced acute lung injury.