Zhan Yao1,
Shuna Liu1 ,
Chunmei Zheng1,
Qiangwu Li1,
Liya Wang2
1Department of Infectious Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong Province 524001, China;
2Interventional Ward, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong Province 524001, China.
For correspondence:- Shuna Liu
Email: Liushuna_666@163.com Tel:+867592387431
Accepted: 29 June 2023
Published: 31 July 2023
Citation:
Yao Z, Liu S, Zheng C, Li Q, Wang L.
Procyanidin A1 improves sepsis-induced liver injury by inhibiting inflammation. Trop J Pharm Res 2023; 22(7):1411-1415
doi:
10.4314/tjpr.v22i7.8
© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
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.
Keywords: Procyanidin A1, Sepsis, Liver injury, Inflammation, NF-κB pathway