The neuroprotective mechanism of puerarin in the treatment of acute spinal ischemia–reperfusion injury is linked to cyclin-dependent kinase 5

Abstract

Puerarin is shown to exert a variety of pharmacological effects including neuroprotective properties. However, mechanisms of the action are not fully understood. This study was designed to explore the mechanism of puerarin in treatment of acute spinal ischemia–reperfusion injury in rats. Acute spinal ischemia–reperfusion injury was conducted by aortic occlusion in twenty-eight male Sprague-Dawley rats, weighting 230–250g. The animals were randomly divided into four groups. In the animals with puerarin treatment, 50mg/kg of puerarin was injected intraperitoneally after reperfusion, and followed by the same dose of injection every 24h for 2 days. In the animals with roscovitine pre-treatment, 30mg/kg roscovitine was intravenously administrated 60min before spinal ischemia started. After spinal ischemia for 60min followed by 48h of reperfusion, the motor function, spinal infarction volume, apoptosis indices and the activities of Cdk5 and p25 were examined. Acute spinal ischemia–reperfusion resulted in an injury of the spines associated with motor deficit, elevation of Cdk5 and p25 activities, and increase in the spinal apoptosis number and spinal infarction volume. Puerarin improved motor function associated with the decreased apoptosis number, spinal infarction volume, and Cdk5 and p25 activities. The present study indicated that reduction of spinal injury was associated with inhibition of Cdk5 and p25, and that inhibition of Cdk5 and p25 was one of the neuroprotective mechanisms in the puerarin treatment of acute ischemia/reperfusion-induced spinal injury in rats.