Du G H, Zhang J T
Institute of Materia Medica, Peking Union Medical College.
Yao Xue Xue Bao. 1995;30(3):184-90.
In the present experiments, an impairment of memory model was made by cerebral ischemia-reperefusion in mice. Sal A at the dosage of 3 and 10 mg.kg-1 i.v. was shown to improve the impairment of memory function induced by cerebral ischemia-reperefusion in step down and step through tests. In these tests, the number of errors of Sal A treated group was less and the latency was longer than that of control group. Meanwhile, Sal A 3 and 10 mg.kg-1 i.v. was found to reduce the MDA contents in the cortex, hippocampus and striatum of cerebral ischemia-reperfused rats in vivo. Sal A 10-100 nmol.L-1 was shown to inhibit the brain lipid-peroxidation and scavenge the free hydroxyl radical in vitro. These results indicate that the antagonistic effects of Sal A on impairment of learning and memory caused by cerebral ischemia-reperefusion may be related with its anti-oxidant activity.
在本实验中，通过小鼠脑缺血再灌注建立记忆损伤模型。静脉注射剂量为3和10mg·kg-1的丹参酮ⅡA可改善脑缺血再灌注在跳台试验和避暗试验中诱导的记忆功能损伤。在这些试验中，丹参酮ⅡA处理组的错误次数比对照组少，潜伏期比对照组长。同时，发现静脉注射3和10mg·kg-1的丹参酮ⅡA可降低体内脑缺血再灌注大鼠皮质、海马和纹状体中的丙二醛含量。在体外，10-100nmol·L-1的丹参酮ⅡA可抑制脑脂质过氧化并清除游离羟基自由基。这些结果表明，丹参酮ⅡA对脑缺血再灌注引起的学习记忆损伤的拮抗作用可能与其抗氧化活性有关。
