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1.
Chinese Medical Journal ; (24): 2572-2577, 2008.
Article in English | WPRIM | ID: wpr-265894

ABSTRACT

<p><b>BACKGROUND</b>The neuroprotective effect of the cyclooxygenase (COX) inhibitor has been demonstrated in acute and chronic neurodegenerative processes. But its function under cerebral ischemic conditions is unclear. This study was designed to evaluate the neuroprotective efficacy of emulsified flurbiprofen axetil (FA, COX inhibitor) and its therapeutic time window in a model of transient middle cerebral artery occlusion (MCAO) in rats.</p><p><b>METHODS</b>Forty-eight male SD rats were randomly assigned into six groups (n = 8 in each group); three FA groups, vehicle, sham and ischemia/reperfusion (I/R) groups. Three doses of FA (5, 10 or 20 mg/kg, intravenous infusion) were administered just after cerebral ischemia/reperfusion (I/R). The degree of neurological outcome was measured by the neurologic deficit score (NDS) at 24, 48 and 72 hours after I/R. Mean brain infarct volume percentage (MBIVP) was determined with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining at 72 hours after I/R. In three other groups (n = 8 in each group), the selected dosage of 10 mg/kg was administrated intravenously at 6, 12 and 24 hours after I/R.</p><p><b>RESULTS</b>The three different doses of FA improved NDS at 24, 48 and 72 hours after I/R and significantly reduced MBIVP. However, the degree of MBIVP in the FA 20 mg/kg group differed from that in FA 10 mg/kg group. Of interest is the finding that the neuroprotective effect conferred by 10 mg/kg of FA was also observed when treatment was delayed until 12 - 24 hours after ischemia reperfusion.</p><p><b>CONCLUSION</b>COX inhibitor FA is a promising therapeutic strategy for cerebral ischemia and its therapeutic time window could last for 12 - 24 hours after cerebral ischemia reperfusion, which would help in lessening the initial ischemic brain damage.</p>


Subject(s)
Animals , Male , Rats , Cyclooxygenase Inhibitors , Pharmacology , Disease Models, Animal , Flurbiprofen , Pharmacology , Infusions, Intravenous , Ischemic Attack, Transient , Drug Therapy , Pathology , Random Allocation , Rats, Sprague-Dawley , Time Factors
2.
Chinese Journal of Traumatology ; (6): 143-147, 2004.
Article in English | WPRIM | ID: wpr-270262

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of puerarin on the neural function and the histopathological changes after ischemic spinal cord injury in rabbits.</p><p><b>METHODS</b>Thirty male New Zealand white rabbits were randomly divided into three groups as follows: puerarin group (n=10) receiving intravenous infusion of 30 mg/kg puerarin for 10 minutes, control group (n=10) receiving intravenous infusion of the same volume of normal saline as puerarin for 10 minutes, and sham operation group (n=10) undergoing only the surgical exposure of the abdominal aorta. Temporary spinal cord ischemia was induced by infrarenal aortic occlusion for 20 minutes and followed by reperfusion. The neural status was scored with the Tarlov criteria at 8, 12, 24 and 48 hours after reperfusion. All the animals were killed at 48 hours after reperfusion and the spinal cords (L5) were removed immediately for histopathological study.</p><p><b>RESULTS</b>The neural function scores at 8, 12, 24 and 48 hours after reperfusion were higher in the puerarin group and sham operation group than those in the control group (P<0.05). More normal motor neurons in the anterior horn of spinal cord were present in the puerarin group and sham operation group than those in the control group (P<0.01). There was a strong correlation between the final neural function scores and the number of normal motor neurons in the anterior horn of spinal cord (r=0.839, P<0.01).</p><p><b>CONCLUSIONS</b>Puerarin can significantly ameliorate the neural function and the histopathological damages after transient spinal cord ischemia in rabbits.</p>


Subject(s)
Animals , Male , Rabbits , Isoflavones , Pharmacology , Motor Neurons , Pathology , Spinal Cord Ischemia , Drug Therapy , Pathology , Vasodilator Agents , Pharmacology
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