2009Zhongguo yaolixue tongbaoRequires access

Inhibitory effects of xanthotoxol on neutrophil infiltration and brain edema induced by focal cerebral ischemia-reperfusion injury in rats

Xianhua Huang

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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.

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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.

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Available 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.

Key concepts: Ischemia, Medicine, Edema, Infiltration (HVAC), Anesthesia, Reperfusion injury, Cerebral edema, Brain ischemia

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