The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

Abstract

Objective: Neurotransmitter plays a crucial role in ischemia cerebrovascular disease. Study has shown that Dexmedetomidine (Dex) contributes to neuroprotective functions. We thus observed the regulatory effect of Dex on the expressions of Glutamate Receptor-2 (GluR2) and N-Methyl-D-Aspartic Acid (NMDA) receptor 2B (NR2B) in cerebral cortical neurons with an ischemia-reperfusion rat model. Patients and methods: Healthy male SD rats were randomly divided into sham, model and Dex treatment groups (N=20 each). Whole-brain ischemia-reperfusion model was generated by the clipping of bilateral common carotid artery with hypotension. Dex (9 μg/kg) was infused immediately after reperfusion, while the other two groups received equal volume of saline. Morris water maze was employed to detect learning and memory function of rats. Brain tissues were extracted at 6, 24 and 72 h after reperfusion. Immunohistochemistry (IHC) was used to detect GluR2 and NR2B receptor levels, the mRNA levels of which were determined by real-time PCR. Results: The longer escape latency and fewer number of crossing platform in water maze were shown in Model rats group. Cortical GluR2 expression was down-regulated while NR2B level was increased. Dex treatment inhibited escape latency and increased crossing times, along with the rise of cortical GluR2 expression and reduction of NR2B expression (p<0.05) in a time-dependent manner (p<0.05). Conclusion: Dex could alleviate ischemia-reperfusion injury of rat brain via down-regulating GluR2 while increasing NR2B expression.