目的研究蛇床子素对大鼠局灶性脑缺血再灌注损伤的保护作用。方法利用大鼠大脑中动脉短暂阻塞(MCAO)造成局灶性脑缺血(2h)再灌注(24h)损伤模型，缺血后1h舌下iv给予蛇床子素5、10mg/kg，再灌注24h，检测大鼠神经功能行为缺陷评分、脑水肿和脑梗死范围，测定脑组织中Na+，K+-ATP酶、Ca2+-ATP酶的活性和髓过氧化物酶(MPO)的活性及用放免法测定脑组织中白细胞介素-8(IL-8)的量。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，减轻脑水肿和降低脑梗死范围，增强Na+，K+-ATP酶和Ca2+-ATP酶活性，降低脑组织中MPO的活性和IL-8的量。结论蛇床子素对脑缺血再灌注损伤有保护作用，其机制可能与蛇床子素抑制大鼠脑缺血再灌注后炎症反应和减轻脑水肿有关。

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.

国家自然科学基金资助项目（30560172）