Inhibitory effects of xanthotoxol on neutrophil infiltration and brain edema induced by focal cerebral ischemia-reperfusion injury in rats
Xianhua Huang
Abstract
Xianhua Huang
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.
OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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