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目的:血小板活化因子(plateletactivatingfactor,PAF)与缺血再灌注脑损伤有密切关系。利用PAF受体拮抗剂WEB2086有助于对PAF、炎性细胞浸润及一氧化氮在脑缺血再灌注损伤中的作用和机制进行深入研究。方法:采用线栓法制成大鼠大脑中动脉缺血再灌注模型,研究PAF对缺血再灌注脑损伤的影响。结果:PAF受体拮抗剂WEB2086对缺血再灌注脑组织一氧化氮的产生有明显的影响,且可明显改善缺血再灌注脑组织的局部脑血流量(regionalcerebralbloodflow,rCBF)和显著降低髓过氧化物酶(myeloperoxidaseofleukocytes,MPO)活性缺血再灌注24h一氧化氮浓度从3.94μmmol/L下降到1.62μmmol/L;rCBF从85.8mL/(min·100g)上升到93.8mL/(min·100g);MPO从3.24U/g下降到2.32U/g,最终减轻局部缺血再灌注脑损伤。结论:PAF受体拮抗剂WEB2086对缺血再灌注脑组织的保护作用与一氧化氮有关。
OBJECTIVE: Platelet activating factor (PAF) is closely related to cerebral ischemia-reperfusion injury. The use of the PAF receptor antagonist WEB2086 helps to further investigate the role and mechanism of PAF, inflammatory cell infiltration and nitric oxide in cerebral ischemia-reperfusion injury. Methods: Rat middle cerebral artery occlusion (MCAO) model was established by thread occlusion and the effect of PAF on brain injury after ischemia reperfusion was studied. Results: PA20 receptor antagonist WEB2086 had a significant effect on the production of nitric oxide in brain tissue after ischemia-reperfusion, and could significantly improve the regional cerebral blood flow (rCBF) and significantly reduce the myelodysplastic syndromes The concentration of nitric oxide decreased from 3.94μmmol / L to 1.62μmmol / L at 24h after reperfusion, while the rCBF increased from 85.8mL / (min · 100g) to 93.8mL / (min · 100g) during myeloperoxidase of leukocytes (MPO) ; MPO decreased from 3.24U / g to 2.32U / g, eventually reducing the ischemic reperfusion brain injury. CONCLUSION: The protective effect of PA20 receptor antagonist WEB2086 on cerebral ischemia / reperfusion injury is related to nitric oxide.