Therapeutic neuroprotective effects of ginkgolide B on cortex and basal ganglia in a rat model of transient focal ischemia.

Cerebral ischemia and reperfusion is one of the leading causes for death and severe disabilities in the world and often lead to irreversible brain damage over later lifespan. The aim of this study was to investigate the evolution of pathological damage in cerebral cortex and basal ganglia following ischemia and to evaluate the therapeutic neuroprotective effect of ginkgolide B in a rat model of stroke induced by middle cerebral artery occlusion (MCAO). TTC stain, brain water content and Evans-Blue extravasation were used to quantify brain damage. Our results demonstrated that basal ganglia undergo progressive pathological damage earlier following MCAO, and injury was stable and irreversible after 5 h following ischemia. However, onset of ischemia injury in cerebral cortex appeared later than basal ganglia and became evident about 3 h following MCAO, and injury was stable and irreversible after 6 h following ischemia. Blood brain barrier opened progressively, and it seemed to be significantly destroyed after 4 h following MCAO comparing with 0 h. Post-ischemic treatment with ginkgolide B improved neurological function and reduced infarct size in basal ganglia within 3 h and cerebral cortex within 5 h following MCAO. The therapeutic effect of ginkgolide B on extenuate brain edema and decrease blood brain barrier permeability were extended for 5h after ischemia, and more evident reversal effect were observed when administrated at earlier time.