Autophagy and ER stress in LPS/GalN‑induced acute liver injury

Numerous mechanisms and factors have been implicated in liver damage; however, the involvement of autophagy and endoplasmic reticulum (ER) stress during early‑stage liver injury remains to be fully elucidated. The present study was conducted to determine the expression of autophagy and ER‑stress‑associated proteins in hepatic tissues following injury. A murine model of liver injury was induced by intraperitoneally injecting lipopolysaccharide (LPS) and D‑galactosamine (GalN), and control mice were similarly injected with normal saline. The gross and histological appearance of the liver was examined, serum alanine aminotransferase (ALT) levels were detected, and protein expression evaluated via Western blot analysis. Co‑administration of LPS and GalN effectively induced liver injury in mice, with severe liver damage manifesting at 6 h following induction. Furthermore, upregulation of autophagy‑associated proteins, including microtubule‑associated protein 1 light chain 3 (MAP1 LC3 or, briefly, LC3‑II) and Beclin 1, were detected 3 h following liver injury. Consistently, the expression of the ER stress factor CCAAT/enhancer binding protein (C/EBP)‑homologous protein decreased after 1 h, but increased 3 h after liver damage. Autophagy and ER stress occurred in early‑stage liver injury induced by LPS‑GalN administration in mice. Induction of autophagy may act as a compensatory mechanism during early liver injury.