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.