蛇床子素对大鼠脑缺血/再灌注损伤的保护作用及其机制

目的研究蛇床子素对大鼠脑缺血/再灌注损伤的保护作用及其机制。方法采用短暂阻塞大鼠大脑中动脉制备局灶性脑缺血(2h)再灌注(24h)损伤模型,缺血后1h分别舌下静脉注射蛇床子素5和10mg·kg-1,再灌注24h,按Longa法对大鼠神经功能行为缺陷进行评分后,用干湿重法测定大鼠脑水肿;测定缺血区脑组织中IL-1β、IL-8、NO的含量和髓过氧化物酶(MPO)、诱导型一氧化氮合酶(iNOS)的活性。结果蛇床子素能改善大鼠脑缺血/再灌注后神经功能行为缺陷评分,减轻脑水肿,降低大鼠脑组织中IL-1β、IL-8和NO含量,抑制脑组织中MPO和iNOS的活性。结论蛇床子素对脑缺血/再灌注损伤有保护作用,作用机制可能与其抑制炎症反应有关。

Protective effects of Osthole on cerebral ischemia-reperfusion injury in rats and its mechanism

Aim To investigate the protective effects of Osthole(Ost)on cerebral ischemia-reperfusion injury in rats and its mechanism.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.5 and 10 mg·kg-1 Ost was injected respectively through sublingual vein 1 hour after the onset of ischemia.At 24 hours of reperfusion,the influence of Ost on neurological deficit score and brain edema were observed;the activities of iNOS and myeloperoxidasse(MPO)in the ischemic hemisphere cortex of the middle cerebral artery area were assayed by spectrophotometry;the content of nitric oxide(NO),interleukin-1beta(IL-1β)and interleukin-8(IL-8)was detected with spectrophotometry and radioimmunoassay respectively.Results Ost significantly reduced the neurological deficit score and the brain edema,inhibited the iNOS and MPO activity,and decreased the contents of NO,IL-1β and IL-8 in the brain tissue.Conclusion Ost had protective effects on cerebral ischemia-reperfusion injury in rats,and its mechanism might be partly due to the inhibition of inflammation induced by ischemia-reperfusion.