Compound Ammonium Glycyrrhizin Protects Hepatocytes from Injury Induced by Lipopolysaccharide/Florfenicol through a Mitochondrial Pathway

摘要

Florfenicol (FFC), a widely used drug for chicken diseases, can aggravatelipopolysaccharide (LPS) damage to the liver. For this condition, natural or synthetic productsdisplaying strong antioxidant capacity are expected to prevent LPS/FFC from inducing liver injury,so in our study, the compound ammonium glycyrrhizin (CAG) is used as the protective drug todecrease the injury to liver. The research aims to illustrate the underlying mechanism of combiningLPS with FFC-induced liver injury and the protective role of CAG by using primary chickenhepatocytes as an in vitro model. The results show that LPS/FFC induced cell apoptosis andCAG protected hepatocytes from injury. The permeability of the cell membrane is elevated byLPS/FFC, leading to the efflux of enzymes (ALT, AST). Flow cytometry analysis indicates thatLPS/FFC treatment increased the apoptosis rate significantly. Furthermore, with the up-regulation ofapoptosis genes bax, cytochrome c and the down-regulation of bcl-2, caspase-3 and caspase-9 areactivated at the gene level. LPS/FFC-induced mitochondrial damage is accompanied by a significantdecrease in mitochondrial membrane potential (MMP) and severe mitochondrial damage. However,CAG improves the situation for the purpose of protecting the liver. In conclusion, it is speculatedthat LPS/FFC induces severe liver injury through apoptosis and the CAG protects hepatocytes frominjury via the mitochondria-mediated apoptosis pathway.