Article Sidebar
Published:
Aug 21, 2022Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
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
