Article Sidebar
Published:
Aug 19, 2023DOI:
10.4314/tjpr.v22i7.8Keywords:
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
Procyanidin A1 improves sepsis-induced liver injury by inhibiting inflammation
Abstract
Purpose: To determine the effect of procyanidin A1 (PCA1) on sepsis.
Methods: Dulbecco’s Modified Eagle Medium (DMEM) was employed to incubate mouse hepatic cell line AML12. The AML12 cells treated with lipopolysaccharide (LPS, 50 μg/mL) was used to establish a sepsis cell model. Cell viability was evaluated using CCK-8 assay, while cell apoptosis was assessed by flow cytometry. Aspartate transaminase (AST), alanine aminotransferase (ALT), IL-6 and TNF-α levels were evaluated by enzyme linked immunosorbent assay (ELISA). Protein expressions were assessed using western blot assay.
Results: The viability of AML12 cells decreased following treatment with IL-1β, but this change was offset by PCA1 treatment (40 or 80 μM). Similarly, cell apoptosis was enhanced after LPS treatment, but this change was attenuated by PCA1 treatment. The AST, ALT, IL-6 and TNF-α levels were all elevated after LPS treatment, but these changes were also reversed by PCA1 treatment, indicating that PCA1 suppressed LPS-induced liver injury and inflammation. Furthermore, the protein levels of p-p65/p65 and p-IκBα increased, and IκBα lowered following LPS treatment, but these effects were reversed by PCA1 treatment, indicating that PCA1 retarded NF-κB pathway.
Conclusion: PCA1 alleviates sepsis-induced liver injury by inhibiting inflammation through NF-κB pathway. This suggestes that PCA1 may be an therapeutic agent for the treatment of sepsis.
