Abstract
Background: The study sought to investigate the effects of dexmedetomidine on cognitive function after anesthesia and to examine its actual mechanism. Methods: A total of 48 rats were randomly divided into model Groups A, B, C, or D. Rats in Groups A, B, and C received a hypodermic injection of D-gal with a concentration of 1,000 mg·kg−1·d−1 respectively for 1 week. Group D received the same volume of saline. The Morris water maze (MWM) test was performed within 6 days of the injection. After the behavior test, Group A received an inhalation dose of 2% sevoflurane. Group B received an inhalation dose of 2% sevoflurane and an intraoperative infusion of dexmedetomidine with a concentration of 10 μg·kg−1·h−1. Group C served as the control group and received no treatment. Group D received an inhalation dose of 2% sevoflurane. Results: In relation to the model establishment, we found that there was no significant difference in body weight and swimming speed before and after modeling. There was no statistically significant difference in the escape latency between Groups A, B, C, and D before modeling. After modeling, there was no statistical difference in the escape latency between Groups A, B, and C, but the difference was statistically significant when compared to Group D (P<0.05). In relation to the dexmedetomidine intervention, we found that compared to Group C, MWM test performance in Group A and B was considerably worse (longer escape latencies and fewer platform crossings within 90 seconds), and were more significant in Group A. .Compared with Group D, the levels of IL-1, IL-6, and TNF-α of the brain homogenates were elevated, and this elevation was highest in Group A, followed by Group B; The pathological changes were consistent with changes in behavioral tests. In group A, there were obvious disorders of glial cell arrangement, apoptosis and deletion. There was no significant change in group D. And the changes of vertebral cells in group B and group C were slight, with orderly arrangement and intact cell structure.Conclusions: Dexmedetomidine inhibits the apoptosis of hippocampal cells and reduces the cognitive dysfunction of rats with MCI induced by D-galactose via the inhibition of the release of inflammatory cytokines.