High-Mobility Group Box 1 Protein Regulates Autophagy in LO2 Cells Following Anoxia-Reoxygenation Injury

The mechanisms of autophagy during liver ischemia-reperfusion injury are not completely understood. This study aimed to assess the role of high-mobility group box 1 protein (HMGB1) in autophagy in LO2 cells following anoxia-reoxygenation injury. LO2 cells were pretreated with the HMGB1 inhibitor ammonium glycyrrhizinate (1000 μmol/L) or the HMGB1 agonist recombinant HMGB1 (rHMGB1, 10 ng/mL) at proper concentrations before induction of anoxia-reoxygenation injury. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and cell viability were evaluated. Then, the expression levels of LC3 and Beclin-1, which are classical autophagy markers, were assessed by Western blot. Autophagosomes were detected by electron microscopy. Our results showed that rHMGB1-treated cells had increased AST and ALT levels in the culture medium, aggravated cell injury, enhanced expression of beclin-1 and LC3 proteins, and increased number of autophagosomes. However, glycyrrhizinate treatment alleviated ALT and AST levels in culture medium, relieved cell injury, reduced beclin-1 and LC3 protein expression levels, and decreased autophagosome number. These findings indicated that HMGB1 likely regulates autophagy in LO2 cells exposed to anoxia-reoxygenation injury.