Effect of perioperative infection factor on apoptosis in hippocampal neurons after surgery in mice

Abstract

Objective To evaluate the effect of the perioperative infection factor on apoptosis in hippocampal neurons after surgery in mice. Methods Ninety-six healthy male C57BL/6 mice, aged 8-10 weeks, weighing 20-25 g, were divided into 4 groups (n=24 each) using a random number table: control group (group C), surgery group (group S), infection group (group I) and infection + surgery group (group I+ S). Open reduction and internal fixation was performed after tibial fracture was induced in S and I+ S groups.In I and I+ S groups, lipopolysaccharide 100 μg/kg was injected intraperitoneally at 1 day and 2 h before surgery and 1, 2 and 3 days after surgery once a day for 5 consecutive days.At 1 and 3 days after surgery, 12 mice in each group were selected to perform the contextual fear conditioning test, and the rate of time spent freezing was recorded to evaluate the cognitive function.At 1 day after surgery, venous blood samples were collected for determination of concentrations of adrenocorticotrophin in serum and corticosterone in plasma.After the contextual fear conditioning test, the mice were sacrificed, and the hippocampi were removed to detect the neuronal apoptosis and expression of activated caspase-3, activated poly(ADP-ribose) polymerase-1, Bax and Bcl-2.The apoptosis index and ratio of Bax to Bcl-2 were calculated. Results Compared with group C, the rate of time spent freezing was significantly decreased (P 0.05). Compared with group S, the rate of time spent freezing was significantly decreased, the concentrations of adrenocorticotrophin in plasma and corticosterone in serum were increased, the apoptosis index and Bax/Bcl-2 ratio were increased, and the expression of activated caspase-3 and poly(ADP-ribose) polymerase-1 was up-regulated in group I+ S(P<0.01). Conclusion The mechanism by which perioperative infection factor aggravates postoperative cognitive dysfunction is related to induction of apoptosis in hippocampal neurons through enhancing stress responses in mice. Key words: Bacterial infections; Intraoperative period; Postoperative complications; Cognition disorders; Apoptosis; Hippocampus; Neurons