Related Experiment Video
Updated: Sep 4, 2025
Acquisition of Resting-State Functional Magnetic Resonance Imaging Data in the Rat
Published on: August 28, 2021
The effects of dexmedetomidine on the cognitive function of mild cognitive impairment (MCI) rats
Qian Zhou1,2, Dongjin Xie3, Ting Chen1,2
1Department of Anesthesiology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Background:
The study sought to investigate the effects of dexmedetomidine (DEX) on cognitive function after anesthesia and to examine its actual mechanism.
Methods:
A total of 48 rats were injected with d-galactose (D-gal) 1,000 mg·kg-1·d-1 and normal saline at the neck and back for 1 week to establish rats with mild cognitive impairment (MCI) and conduct behavioral tests. Sevoflurane was inhaled and DEX was pumped into each group respectively. Morris water maze (MWM) test was conducted 24 hours later. The inflammatory factors interleukin (IL)-1, interleukin (IL)-6, and a tumor necrosis factor (TNF)-α in brain homogenate were quantitatively measured by enzyme-linked immunosorbent assay (ELISA) on the next day. The apoptosis of hippocampal cells was observed by hematoxylin-eosin staining (HE staining).
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 DEX intervention, we found that compared to Group C, MWM test performance in Groups 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 inflammatory cytokines 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:
DEX inhibits the apoptosis of hippocampal cells and reduces the cognitive dysfunction of rats with MCI induced by D-gal via the inhibition of the release of inflammatory cytokines.
