serofendic-acid and Reperfusion-Injury

Serofendic acid is a low-molecular-weight compound extracted from fetal calf serum. We previously reported that intracerebroventricular administration of serofendic acid prevents cerebral ischemia-reperfusion injury. However, the effect of peripheral administration of serofendic acid on cerebral ischemia-reperfusion injury has not been examined. In the present study, we investigated the effect of intravenous administration of serofendic acid against cerebral ischemia-reperfusion injury using transient middle cerebral artery occlusion model rats. Serofendic acid (10mg/kg) administrated three times, including 30min before the onset of ischemia, just after the onset of ischemia and just before reperfusion reduced the infarct volume and improved the neurological dysfunction induced by ischemia-reperfusion without affecting regional cerebral blood flow or physiological parameters. However, there were no protective effects when serofendic acid (30mg/kg) was only administered once at 30min before the onset of ischemia, just after the onset of ischemia, or just before reperfusion. Our results reveal the importance of maintaining the blood concentration of serofendic acid for preventing cerebral ischemia-reperfusion injury.

Topics: Administration, Intravenous; Animals; Brain; Brain Ischemia; Diterpenes; Male; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Reperfusion Injury

We previously reported that a sulfur-containing neuroprotective substance named serofendic acid purified and isolated from fetal calf serum prevented glutamate neurotoxicity in rat cortical cultured neurons. In the present study, we investigated the effect of serofendic acid on ischemic injury induced by a transient occlusion of the middle cerebral artery in rats. Serofendic acid was intracerebroventricularly administered 30 min after the onset of the occlusion. Serofendic acid (30 nmol) significantly reduced total infarct volume, similar to edaravone (30 nmol), a free radical scavenger. Treatment with serofendic acid (1-30 nmol) reduced the infarct volume in a dose-dependent manner. Moreover, serofendic acid (30 nmol) improved neurological deficit scores. These results suggest that intracerebroventricular administration of serofendic acid prevents the neurodegeneration induced by a transient focal cerebral ischemia and reperfusion.

Topics: Animals; Antipyrine; Body Weight; Brain Ischemia; Cerebrovascular Circulation; Diterpenes; Dose-Response Relationship, Drug; Edaravone; Infarction, Middle Cerebral Artery; Male; Middle Cerebral Artery; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Reperfusion Injury