目的 观察总丹酚酸 (Sal)对脑缺血再灌注损伤的保护作用。方法 采用小鼠和大鼠脑缺血再灌注模型。结果 在小鼠和大鼠全脑缺血再灌注模型上,Sal10,2 0 m g/ kg iv及 Sal5,10 mg/ kg iv可显著提高脑组织乳酸脱氢酶 (L DH)及超氧化物歧化酶 (SOD)活性,明显降低丙二醛 (MDA)含量。在大鼠局灶性脑缺血 2 h再灌注 2 4h模型上,Sal 5,10 mg/ kg iv可明显缩小梗死灶面积,改善神经功能缺损,并显著抑制缺血脑组织中 L DH和 SOD活性降低,减少 MDA的过量产生。结论 Sal对小鼠和大鼠脑缺血再灌注损伤有显著保护作用,其机制与其抗氧自由基作用有关

Obj ect It was reported that salvianolic acid A from Salvia miltio rrhiza Bge. could improve memory dysfunction of mice with cerebral isch emia-reperfusion injury. The effects of total salvianolic acids (Sal), includi ng salvianolic acid A and B, rosmaric acid and protocatechic aldehyde was now st udied to observe its effect on cerebral ischemia-reperfusion injury in hope of obtaining a preliminary view on its mechanism of action. Methods The effects of Sal on lactic dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) of cerebral ischemia-reperfusion injured mouse and ra t models were observed. Results Sal 10, 20 mg/kg iv and 5, 10 mg/kg iv could markedly increase the activities of LDH and SOD and lower the pr oduction of MDA in the injured cerebral tissue. On focal cerebral ischemia repe rfusion injured rat, 24 h reperfusion after 2 h ischemic injury, 5, 10 mg/kg iv Sal could decrease infarct size, ameliorate neurological deficit with obvious i nhibition of the decrease of LDH and SOD activities and the over production of M DA. Conclusion Sal showed obvious protective effects on cereb ral ischemia reperfusion injuries of mice and rats via attenuating oxygen free r adical.

国家科委“1035”工程新药基金资助项目,(No.K95-12-27)