目的探讨银杏二萜内酯葡胺注射液(DGMI)对缺血性脑卒中的保护作用、治疗时间窗及相关机制。方法制备大鼠大脑中动脉阻塞(t MCAO)模型,缺血1 h后ip不同剂量的DGMI(1.25、2.50、5.00、10.00 mg/kg),缺血1.5 h后血流复灌,再灌注24和72 h评价大鼠神经运动功能,72 h时测定脑梗死体积、脑组织含水量以及氧化应激和IL-1β水平;选取DGMI有效剂量5.0 mg/kg,分别于再灌注前0.5 h、再灌后1、2、3和6 h时给药,3 d后取材研究药物治疗时间窗。结果2.5、5.0 mg/kg剂量的DGMI改善大鼠再灌注24 h后的神经运动功能、减小脑梗死体积、减轻脑水肿、增强缺血脑组织的超氧化物歧化酶(SOD)的活力,减弱肌酸激酶(CK)、乳酸脱氢酶(LDH)的活力,降低丙二醛(MDA)、IL-1β水平。DGMI5.0 mg/kg在t MCAO大鼠再灌注3 h内给药均改善神经运动功能障碍、减小脑梗死体积、减轻脑水肿。结论 DGMI对大鼠缺血性脑卒中急性期损伤具有保护作用,治疗时间窗少于缺血再灌注后6 h,其机制与抗氧化应激、抑制炎症相关。 Objective To investigate the protective effect of ginkgo diterpene lactone meglumine injection (DGMI) on ischemic stroke, the treatment time window and related mechanisms. Methods Rat middle cerebral artery occlusion (t MCAO) model was established. After 1 h ischemia, different doses of DGMI (1.25, 2.50, 5.00 and 10.0 mg / kg) And 72 h respectively. The cerebral infarction volume, brain tissue water content, oxidative stress and IL-1β level were measured at 72 h. The effective dose of DGMI 5.0 mg / kg was selected before 0.5 h reperfusion 1, 2, 3 and 6 h after the administration, after 3 d drawn study drug treatment time window. Results DGMI of 2.5 and 5.0 mg / kg could improve the motor function, reduce the volume of cerebral infarction, relieve cerebral edema and increase the activity of superoxide dismutase (SOD) in ischemic brain tissue 24 hours after reperfusion, Weaken the activity of creatine kinase (CK) and lactate dehydrogenase (LDH) and lower the levels of malondialdehyde (MDA) and IL-1β. Administration of DGMI 5.0 mg / kg within 3 h after reperfusion in t MCAO rats ameliorates neuromotor dysfunction, decreases the volume of cerebral infarction, and decreases brain edema. Conclusion DGMI has a protective effect on acute ischemic stroke in rats. The treatment time window is less than 6 h after ischemia-reperfusion, and its mechanism is related to anti-oxidative stress and inhibition of inflammation.