Compound ammonium glycyrrhizin (CAG) protects hepatocytes from injury induced by lipopolysaccharide (LPS)/florfenicol (FFC) through a mitochondrial pathway. On this basis, the research was aimed to investigate whether CAG protects hepatocytes from injury induced by LPS/FFC through oxidative stress and the MAPK pathway. For liver injury induced by LPS/FFC, not only CAG can protect hepatocytes and prevent membrane permeability from being increased, but also the activities of ALT and AST were decreased significantly by CAG. Flow cytometry analysis indicated that the apoptosis rate (35.65 ± 2.48%) of LPS/FFC group was significantly higher than that of the control group (8.60 ± 0.32%). CAG (concentration of 0.01 μg/mL, 0.1 μg/mL, 1 μg/mL) significantly decreased the apoptosis rate (23.69 ± 0.54%, 14.92 ± 2.45% and 9.47 ± 1.28%) for the liver injury induced by LPS/FFC. The activities of SOD and GSH were increased with the increased concentration of CAG, and the activity of MDA was decreased with the increased concentration of CAG. All the mRNA and proteins expression levels were increased by LPS/FFC-induced liver injury which associated with the MAPK pathway, and those of the CAG group were decreased with the increased concentration of CAG. And the change of caspase-3 activity was consistent with that of proteins and mRNA. It is suggested that LPS/FFC can induce liver injury through apoptosis and the CAG can protect hepatocytes from injury through the MAPK pathway and oxidative stress.
Keywords: Apoptosis; Compound ammonium glycyrrhizin; Liver injury; Oxidative stress; The MAPK pathway.
Copyright © 2019. Published by Elsevier Inc.