SOD2 overexpression in bone marrow‑derived mesenchymal stem cells ameliorates hepatic ischemia/reperfusion injury.

Hepatic ischemia/reperfusion injury (HIRI) is a complex pathophysiological process that may develop after liver transplantation and resection surgery, as well as in uncontrolled clinical conditions. Bone marrow‑derived mesenchymal stem cells (BM‑MSCs) are potential targets for liver diseases. Thus, the present study aimed to investigate the effects of superoxide dismutase 2 (SOD2) overexpression in BM‑MSCs on HIRI by constructing a HIRI rat model. The adenoviral vector containing SOD2 and the corresponding control vector were designed and constructed, and SOD2‑overexpressing BM‑MSCs were injected into the tail vein of the rats. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, as well as pathological changes and the remnant liver regeneration rate were determined. The activities of SOD and glutathione peroxidase (GSH‑Px), and malondialdehyde (MDA) content were measured. Reactive oxygen species (ROS) were determined with 2',7'‑-dichlorofluorescein diacetate and measured via fluorescence microscopy. Cell apoptosis was assessed using TUNEL staining. Moreover, the expression levels of Bax, Bcl‑2 and caspase‑3 were detected via western blotting. SOD2‑overexpressing BM‑MSCs significantly reduced the elevation of serum AST and ALT levels. Furthermore, SOD2‑overexpressing BM‑MSCs enhanced SOD and GSH‑Px activities, and suppressed the production of MDA and ROS. Histopathological findings revealed that SOD2‑overexpressing BM‑MSCs decreased the number of TUNEL‑positive cells in the liver. It was also found that SOD2‑overexpressing BM‑MSCs promoted Bcl‑2 expression, but inhibited Bax and caspase‑3 expression in HIRI. Collectively, these findings suggest that SOD2‑overexpressing BM‑MSCs may provide therapeutic support in HIRI by inhibiting oxidative stress and hepatocyte apoptosis.