Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization
Ischemia is a condition in which blood flow (and thus oxygen) is restricted or reduced in a part of the body.
Introduction:
The pathophysiology of
cerebral ischemia is essential for early diagnosis, neurologic recovery, the early onset of drug treatment and the prognosis of ischemic events. Experimental models of cerebral ischemia can be used to evaluate the cellular response phenomena and possible neurological protection by drugs.
Cerebrovascular disease (CVD) is the leading cause of permanent disability and the third leading cause of death in Colombia and in the world. Cerebral ischemia represents 85% of CVD, causing about
6,000,000 deaths per year. CVD causes cellular death by various mechanisms, with obstructive type ischemia being the most frequent, caused by a clot that occludes one or more branches of a major artery, usually the middle cerebral artery.
Dimethyl Sulfoxide (DMSO) has been used in biological research as a solvent of hydrophobic substances and used successfully in the treatment of rheumatic, musculoskeletal, dermatological, gastrointestinal and urinary tract disorders for its anti-inflammatory and antioxidant properties.
Since DMSO can cross the blood-brain barrier (BBB), it has been used to treat cerebral edema; it has potential neuroprotective actions, such as the capture of free radicals and inhibition of prostaglandin and vasodilatation receptors.
Objective:
To characterize the cellular changes in the neuronal population and astrocytic response by the effect of Dimethyl Sulfoxide (DMSO) on a model of ischemia caused by cerebral embolism.
Results:
Cerebral embolism induced reproducible and reliable lesions in the cortex and hippocampus (CA1)., similar to those of focal models. DMSO did not reverse the loss of post-ischemia neuronal immune-reactivity, but prevented the morphological damage of neurons, and significantly reduced astrocytic hyperactivity in the somato-sensory cortex and CA1 (p <0.001).
Conclusions
The regulatory effect of DMSO on astrocyte hyperreactivity and neuronal-astroglial cytoarchitecture , gives it potential neuroprotective properties for the treatment of thromboembolic cerebral ischemia in the acute phase.
DMSO significantly reduces astrocytic hyper-reactivity (gliosis) in the areas of the cerebrum affected by arterial embolization and, although it does not diminish the loss of neuronal immune reactivity, it prevents the changes in cytoarchitecture that might be related to neurotoxicity.The regulatory effect of DMSO on astrocytes and neurons after arterial embolization potentially confers neuroprotective properties for the treatment of thromboembolic cerebral ischemia in the acute phase.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4002012/