A mouse model of hepatic ischemia-reperfusion injury demonstrates potentially reversible effects on hippocampal neurons anpostoperative cognitive function

Abstract

Background: This study aimed to investigate cognitive function, hippocampal neuronal changes, and the expression of inflammatory 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 I/R1 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-kB (NF-kB) and choline acetyl-transferase (ChAT) were quantified by immunohistochemistry. Serum tumor necrosis factor-a (TNF-a) and in-terleukin-1b (IL-1b) were measured by enzyme-linked immunosorbent assay (ELISA). Results: Groups I/R1 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. Conclusions: The I/R2 group showed reduced numbers of Nissl bodies in hippocampal neurons. The I/R1 and I/R2 groups had increased expression of NF-kB, TNF-a, and IL-1b and decreased ChAT. No differences between the groups were found in levels of NF-kB, TNF-a, IL-1b, or ChAT by day 18. A mouse model of hepatic ischemia-reperfusion injury showed transient and reversible cognitive dysfunction, changes in hippocampal neurons, and expression of inflammatory cytokines.