Article Sidebar
Published:
Jun 11, 2023Keywords:
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
Decursinol angelate attenuates lipopolysaccharide induced acute lung injury by regulating AKT/NF κB pathway
Abstract
Purpose: To investigate the effect of decursinol angelate in acute lung injury induced by lipopolysaccharide treatment.
Methods: Human bronchial epithelial cells (BEAS-2B cells) and human pulmonary artery endothelial cells (HPAECs) were exposed to lipopolysaccharide to induce cell injury and then treated with 20, 40, or 60 μM decursinol angelate. Cell viability was quantified using a cell counting assay, while cell apoptosis was evaluated by western blot and flow cytometry. Colorimetric and enzyme-linked immunosorbent assay (ELISA) was used to measure oxidative stress. Expressions of tumor necrosis factor-alpha (TNF-α), interleukin-1β, and interleukin-6 were evaluated using quantitative real-time-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Phosphorylation levels of p65, IκBα, AKT, and phosphatidylinositol 3-kinase were assessed by western blot, while the entry of p65 into the nucleus was investigated by indirect immunofluorescence assay.
Results: Treatment with 40 or 60 μM decursinol angelate increased cell viability after lipopolysaccharide-induced damage. B-cell lymphoma 2 (Bcl2) and Bax expression were regulated, and the rate of apoptosis was inhibited. The concentration of superoxide dismutase and glutathione was elevated, and the density of malondialdehyde and myeloperoxidase decreased significantly. Inflammation was also suppressed by decursinol angelate by regulating TNF-α, interleukin-1β, and interleukin-6 expressions. Furthermore, decursinol angelate significantly decreased the phosphorylation of p65, IκBα, AKT, and phosphatidylinositol 3-kinase. Finally, decursinol angelate inhibited p65 entry into the cell nucleus.
Conclusion: Decursinol angelate alleviates cell damage and apoptosis, reduces oxidative stress, and attenuates inflammation after lipopolysaccharide-induced acute lung injury by inhibiting AKT/NF-κB signaling pathway. Thus, decursinol angelate is a potential candidate for the treatment of lung injury.
