The Effect of Dexmedetomidine on Oxidative Stress Response Following Cerebral Ischemia-Reperfusion in Rats and the Expression of Intracellular Adhesion Molecule-1 (ICAM-1) and S100B

Yanwen Li, Shikun Liu, Yanwen Li, Shikun Liu

Abstract

BACKGROUND Ischemia-reperfusion injury of whole brain involves a complicated pathophysiology mechanism. Dexmedetomidine (Dex) has been shown to have neuro protective functions. This study observed the effect of Dex on serum S100B and cerebral intracellular adhesion molecule-1 (ICAM-1) in a rat model of cerebral ischemia-reperfusion. MATERIAL AND METHODS Healthy Sprague Dawley (SD) rats (males, 7 weeks old) were randomly divided into sham, model, and Dex groups (n=20 each). A cerebral ischemia-reperfusion model was prepared by clipping of the bilateral common carotid artery combined with hypotension. Dex (9 μg/kg) was infused intravenously immediately after reperfusion in the Dex group, while the other two groups received an equal volume of saline. Neural defect score (NDS) was measured at 6 hours, 24 hours, and 72 hours after surgery, with pathological observation of brain tissues. ELISA was then used to test serum S100B protein level. Malondialdehyde (MDA) and superoxide dismutase (SOD) were assayed by spectrometry. Nuclear factor-kappa B (NF-kB) and ICAM-1 levels were determined by real-time (RT)-PCR. RESULTS Model rats had significant injury in the hippocampal CA1 region as shown by elevated NDS, S100B, and MDA levels, higher NF-κB and ICAM-1 mRNA expression, and lower SOD levels (p<0.05). Dex treatment improved pathological injury, decreased NDS, S100B, and MDA levels, decreased expression of mRNA of NF-κB and ICAM-1, and increased SOD levels. CONCLUSIONS Dex alleviated ischemia-reperfusion damage to rat brains, and inhibited NF-κB and ICAM-1 expression in brain tissues, possibly via inhibiting oxidative stress and inflammatory response.

Conflict of interest statement

Disclosure of conflict of interest

The authors declare no competing financial or commercial interests in this manuscript.

Figures

Figure 1
Figure 1
NDS of cerebral ischemia-reperfusion rats. #p<0.05 compared to control group; * p<0.05 compared to model group; & p<0.05 compared to 6 hour group; @p<0.05 compared to 24 hour group.
Figure 2
Figure 2
Morphology of hippocampal CA1 zone (HE staining, ×400).
Figure 3
Figure 3
Cerebral levels of MDA (A) and SOD (B). #p<0.05 compared to control group; * p<0.05 compared to model group; &p<0.05 compared to 6 hour group; @p<0.05 compared to 24 hour group.
Figure 4
Figure 4
Serum S100 protein level. #p<0.05 compared to control group; * p<0.05 compared to model group; &p<0.05 compared to 6 hour group; @p<0.05 compared to 24 hour group.
Figure 5
Figure 5
mRNA expression of NF-κB (A) and ICAM-1 (B). #p<0.05 compared to control group; * p<0.05 compared to model group; &p<0.05 compared to 6 hour group; @p<0.05 compared to 24 hour group.

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