Background: Dimethyl sulfoxide (DMSO) has been used as a solvent for many drugs in ischemic experiments. DMSO has many biological benefits, including antioxidant, anti-inflammatory, platelet aggregation inhibiting and cell membrane stabilizing effects. Moreover, some experimental studies report that DMSO has a neurprotective effect in permanent focal cerebral ischemia. Despite the effect of DMSO on the cortex, striatum injuries and motor neurological dysfunctions in transient focal cerebral ischemia are not completely clear.

Methods: Thirty-six male Sprague-Dawley rats weighing 300-350 g were divided into saline- (control) and DMSO-treated groups. Under chloral hydrate anesthesia (400mg/kg, ip), transient focal cerebral ischemia was induced by 90-min middle cerebral artery occlusion (MCAO) followed by 23-h reperfusion. Rats received saline (n=11) or 2% DMSO intraperitoneally at doses of 0.01 (n=11), 0.1 (n=7) and 0.2 (n=7) ml/kg 30 min prior to induction of ischemia. Twenty-four hours after MCAO, the neurological deficit scores were ascertained. Cortical and striatal infarct volumes determined by triphenyltetra-zolium chloride staining. 

Results: Administration of DMSO at doses of 0.1 and 0.2 ml/kg significantly reduced cortical and striatal infarct volumes (p<0.001), while rats receiving the 0.1 ml/kg dose had infarct volumes similar to those of the control group (p=0.225). Moreover, only 0.2 ml/kg doses of DMSO significantly reduce neurological motor dysfunction (p<0.001).

Conclusions: Findings of this study indicate that DMSO is a potent neuroprotective agent against transient focal cerebral ischemia in rat. Moreover, our data also suggest that DMSO may be a candidate for acute stroke treatment.