A Mouse Model of Hepatic Ischemia-Reperfusion Injury Demonstrates Potentially Reversible Effects on Hippocampal Neurons and Postoperative Cognitive Function

Background: This study aimed to investigate cognitive function, hippocampal neuronal changes, and the expression of in-flammatory cytokines in a mouse model of hepatic ischemia-reperfusion injury. Material/Methods: Sixty mice were divided into the sham group, which underwent surgery without vascular occlusion; the 1/81 group, with occlusion of the left hepatic artery and portal vein for 20 min, and reperfusion for 30 min; and the I/R2 group, with occlusion of the left hepatic artery and portal vein for 40 min, and reperfusion for 30 min. At postoperative day 4 and 11, ten mice from each group underwent the Morris water maze (MWM) task. Hippocampal tissues were stained for Nissl bodies. Expression of nuclear factor-kappa B (NF-kappa B) and choline acetyl-transferase (ChAT) were quantified by immunohistochemistry. Serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) were measured by enzyme-linked immunosorbent assay (ELISA). Results: Groups 1/81 and I/R2 showed a significantly increased latency in the MWM test between days 5-9, compared with the sham group (P<0.05), with no difference by day 11; the I/R2 group had an initial lower crossing frequency (P<0.05), with no difference by day 18. The I/R2 group showed reduced numbers of Nissl bodies in hippocampal neurons. The I/R1 and I/R2 groups had increased expression of NE-kappa B, TNF-alpha, and IL-1 beta and decreased ChAT. No differences between the groups were found in levels of NF-kappa B, TNF-alpha, IL-1 beta, or ChAT by day 18. Conclusions: A mouse model of hepatic ischemia-reperfusion injury showed transient and reversible cognitive dysfunction, changes in hippocampal neurons, and expression of inflammatory cytokines.