Conclusion
Dexmedetomidine could significantly relieve the postoperative cognitive dysfunction in aged rats. The mechanism may be associated with the decreased inflammatory cytokines in the hippocampus.
Methods
A total of 45 aged healthy male Sprague Dawley rats were divided into control group, sham group, and dexmedetomidine group. The open tibia fracture surgery rat model was established, and dexmedetomidine was intraperitoneally injected before operation. The cognitive function of aged rats was examined by Morris Water-Maze Test, open field experiment, and passive avoidance memory test. The expression levels of IL-6, IL-1β, and TNF-α in the hippocampus were examined by enzyme-linked immunosorbent assay (ELISA).
Objective
To investigate the effects of dexmedetomidine on the cognitive dysfunction of aged rats after open tibia fracture surgery and the expression of inflammatory cytokines in the hippocampus.
Results
The escape latency over 5 continuous days in the dexmedetomidine group was significantly shorter than that in the control group (all P<0.05). The number of swimming times and the percentage of swimming time in the dexmedetomidine group were significantly higher and longer than those in the control group (all P<0.05). Moreover, rats in the dexmedetomidine group exhibited shorter time of stay at the central square and higher number of standing times in comparison with the control group (all P<0.05). Compared with the control group, dexmedetomidine intraperitoneally injected before surgery significantly inhibited the expression levels of IL-6, IL-1β, and TNF-α in the hippocampus (all P<0.05).