ABSTRACT
Objective To investigate the protective effect of osthole on focal cerebral ischemia-reperfusion injury in rats.Methods Focal cerebral ischemia-reperfusion model in rat was made by transient occlusion of the middle cerebral artery for 2 h and followed by reperfusion for 24 h.Osthole 5 and 10 mg/kg were iv injected through sublingual vein at 1 h after the onset of ischemia,respectively.After 24 h of reperfusion,the influence of osthole on neurological behaviour deficit score,brain edema,and infarct size were evaluated.The activity of Na+,K+-ATPase,Ca2+-ATPase,and myeloperoxidase(MPO)in the ischemic hemisphere cortex of the middle cerebral artery area was assayed by spectrophotometry.The level of IL-8 was detected with radioimmunoassay.Results Osthole significantly reduced the neurological behaviour deficit score,brain edema,and infarct size,enhanced the activity of Na+,K+-ATPase and Ca2+-ATPase,inhibited the activity of MPO,and decreased the level of IL-8 in the brain tissue.ConclusionThe results suggest that osthole could attenuate the brain damage following focal cerebral ischemia-reperfusion in rats and its mechanism may be partly related to the inhibition of inflammation and brain edema induced by ischemia-reperfusion.
ABSTRACT
Aim To investigate the inhibitory effects of xanthotoxol(XT) on neutrophil infiltration and brain edema induced by focal cerebral ischemia-reperfusion injury in rats.Methods Focal cerebral ischemia-reperfusion model in rat was induced by transient occlusion of the middle cerebral artery for 2 hours and followed by 24 hours of reperfusion.XT(2.5,5 and 10 mg?kg-1,ip)was administered at 1 hour and 12 hours after the onset of ischemia,respectively.After 24 hours of reperfusion,the influence of XT on neurological deficit score,brain edema and infarct size were evaluated;the activity of Na+,K+-ATPase,Ca2+-ATPase and myeloperoxidasse(MPO) in the ischemic hemisphere cortex of the middle cerebral artery area was assayed by spectrophotometry;the expression of intercellular adhesion molecule-1(ICAM-1) and E-selectin was measured with immunohistochemistry.Results XT significantly reduced the neurological deficit score,brain edema and infarct size,enhanced activity of Na+,K+-ATPase and Ca2+-ATPas,suppressed the injury-induced upregulation of MPO activity and cell adhesion molecules(ICAM-1 and E-selectin) expression in the brain tissue.Conclusion XT attenuates brain damage following focal cerebral ischemia-reperfusion in rats and its mechanism may partly be due to the inhibition of inflammation and brain edema induced by ischemia-reperfusion.