ABSTRACT
Introduction:The pathophysiology of cerebral ischemia is essen-tial for early diagnosis, neurologic recovery, the early onset of drugtreatment and the prognosis of ischemic events. Experimental modelsof cerebral ischemia can be used to evaluate the cellular response phe-nomena and possible neurological protection by drugs.Objective:To characterize the cellular changes in the neuronal po-pulation and astrocytic response by the effect of Dimethyl Sulfoxide(DMSO) on a model of ischemia caused by cerebral embolism.Methods:Twenty Wistar rats were divided into four groups (n = 5).The infarct was induced with α-bovine thrombin (40 NIH/Unit.). Thetreated group received 90 mg (100 μl) of DMSO in saline (1:1 v/v) in-traperitoneally for 5 days; ischemic controls received only NaCl (pla-cebo) and two non-ischemic groups (simulated) received NaCl andDMSO respectively. We evaluated the neuronal (anti-NeuN) and as-trocytic immune-reactivity (anti-GFAP). The results were analyzed bydensitometry (NIH Image J-Fiji 1.45 software) and analysis of variance(ANOVA) with the Graph pad software (Prism 5).Results:Cerebral embolism induced reproducible and reliable lesionsin the cortex and hippocampus (CA1)., similar to those of focal mo-dels. DMSO did not reverse the loss of post-ischemia neuronal im-mune-reactivity, but prevented the morphological damage of neurons,and significantly reduced astrocytic hyperactivity in the somato-sen-sory cortex and CA1 (P <0.001).Conclusions:The regulatory effect of DMSO on astrocyte hyperreac-tivity and neuronal-astroglial cytoarchitecture , gives it potential neu-roprotective properties for the treatment of thromboembolic cerebralischemia in the acute phase.