RESUMEN
Background: The number of patients having ischemic stroke is increasing year on year. The anesthetic adjuvant dexmedetomidine is neuroprotective in rats and has potential for use in the treatment of ischemic stroke. Objective: The neuroprotective mechanism of dexmedetomidine in cerebral ischemia-reperfusion injury was studied in relation to its regulation of the oxidative stress response, astrocyte response, microglia overactivation, and apoptosis-related protein expression. Methods: We randomly and equally divided 25 male Sprague-Dawley rats into 5 groups: a sham-operation group, an ischemia-reperfusion injury group, and low-, medium-, and high-dose dexmedetomidine groups. A rat model of focal cerebral ischemia-reperfusion injury was established by embolization of the right middle cerebral artery for 60 minutes and reperfusion for 2 hours. The volume of cerebral infarction was calculated by triphenyl tetrazolium chloride staining. The protein expression levels of caspase-3, methionyl aminopeptidase 2 (MetAP2 or MAP2), glial fibrillary acidic protein, and allograft inflammatory factor 1 (AIF-1) in the cerebral cortex were determined by Western blot and immunohistochemistry. Results: The volume of cerebral infarction in rats decreased with increasing dose of dexmedetomidine (P = .039, 95% CI = .027 to .044). The expression levels of caspase-3, glial fibrillary acidic protein, and allograft inflammatory factor 1 and the amount of 4-hydroxynonenal decreased with increasing doses of dexmedetomidine (P = .033, 95% CI = .021 to .037). Methionyl aminopeptidase 2 (MetAP2 or MAP2) expression increased with increasing doses of dexmedetomidine (P = .023, 95% CI = .011 to .028). Conclusion: Dexmedetomidine has a dose-dependent protective effect on cerebral ischemic injury in rats. The neuroprotective effects of dexmedetomidine are achieved, in part, by reducing the oxidative stress response, inhibiting glial overactivation, and inhibiting expression levels of apoptosis-related proteins.