Chrysoeriol alleviated inflammation in infantile pneumonia by inhibiting PI3K/AKT/mTOR signaling pathway

Abstract

Purpose: To assess the therapeutic effects of chrysoeriol (CHE) on pediatric pneumonia and determine the mechanism of action. Methods: The role of chrysoeriol was investigated in a human lung fibroblasts (HFL1) cell model of pneumonia. The effects of lipopolysaccharide (LPS) and CHE on cell viability and apoptosis were determined by CCK-8 kit and flow cytometry, respectively, while oxidative stress was determined by evaluating the levels of superoxide dismutase (SOD), glutathione, r-glutamyl cysteine +glycine (GSH)- px, myeloperoxidase (MPO) and malondialdehyde (MDA). Inflammatory response was assessed by determining IL-1β, TNF-α, IL-18 and IL-10 levels using enzyme-linked immunosorbent assay (ELISA). The mechanisms of action of CHE were evaluated by immunoblot assays. Results: Chrysoeriol increased the viability of LPS-induced pneumonia cells (p < 0.001) but decreased cell apoptosis (p < 0.001). Furthermore, chrysoeriol reduced oxidative stress and inflammation in LPSinduced pneumonia cells, and suppressed the activation of PI3K/AKT/mTOR pathway. Conclusion: Chrysoeriol alleviates inflammation of infantile pneumonia by inhibiting PI3K/ AKT /mTOR signaling pathway. Thus, CHE is a potential drug for the management of pneumonia. Keywords: Chrysoeriol; Pneumonia; Cell viability; Oxidative stress; PI3K/AKT/mTOR pathway