Research Papers:

Ammonium glycyrrhizin counteracts liver injury caused by lipopolysaccharide/amoxicillin-clavulanate potassium

Zugong Yu _, Feng Wu, Jing Tian, Xuewen Guo, Ran An and Yangyang Guo

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Oncotarget. 2017; 8:96837-96851. https://doi.org/10.18632/oncotarget.18291

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Zugong Yu1, Feng Wu1, Jing Tian1, Xuewen Guo1, Ran An1 and Yangyang Guo1

1Laboratory of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, 210095, China

Correspondence to:

Zugong Yu, email: [email protected]

Keywords: lipopolysaccharide, amoxicillin clavulanate potassium, chicken primary hepatocytes, compound ammonium glycyrrhizin, antioxidant

Received: November 02, 2016     Accepted: May 07, 2017     Published: May 30, 2017


We treated isolated chicken primary hepatocytes with lipopolysaccharide/amoxicillin clavulanate potassium (LPS/AC) to model liver injury and investigate its underlying mechanisms. We also used this model to assess the cytoprotective effects of compound ammonium glycyrrhizin (CAG) in vitro. LPS/AC-induced injury decreased cell viability and increased the activity of serum aspartate transaminase and alanine transaminase. Levels of superoxide dismutase, glutathione, and glutathione peroxidase were lower than control, while levels of the oxidative product malondialdehyde and reactive oxygen species were higher. Treatment with CAG for 24 h ameliorated these changes. Caspase-3 activity assays and flow cytometry revealed increased apoptosis in the model group. However, apoptosis decreased after CAG treatment, as confirmed by Hoechst 33342 staining. We also observed changes in mitochondrial ultrastructure. Real-time PCR and western blot analyses showed that CAG treatment downregulated LPS/AC-induced RNA expression of caspase-3, caspase-9, bax, cytochrome c, and fas, and upregulated the expression of bcl-2. Mitochondrial cytochrome c was released into the cytosol and the inner mitochondrial membrane potential (ΔΨm) was decreased. Our results highlight CAG as a potential therapeutic agent to counteract LPS/AC-induced liver injury.

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