摘要
用脑缺血再灌模型和跳台试验,研究了金丝桃甙(Hyp)对脑缺血再灌损伤的保护作用。结果表明,在小鼠脑缺血再灌模型上,Hyp(50及100mg·kg-1,ip)可显著抑制脑组织乳酸脱氢酶(LDH)活性的下降;表明,Hyp跳台试验对脑缺血再灌致小鼠学习记忆功能障碍有明显的改善作用;在大鼠四血管结扎模型上,Hyp可显著抑制脑组织中LDH、超氧物岐化酶(SOD)及谷胱甘肽过氧化物酶(GSHPx)活性的降低,减少脑组织脂质过氧化产物丙二醛(MDA)和一氧化氮(NO)的含量的增高,并促进EEG变化的恢复。上述结果提示Hyp对脑缺血再灌损伤有显著保护作用,其机制可能与其抗自由基、抑制NO的生成有关。
The protective effect of hyperin (Hyp) against cerebral ischemiareperfusion injury was studied. On the cerebral ischemiareperfusion model in mice, Hyp (50, 100 mg·kg-1, ip) was shown to markedly and dosedependently inhibit the decrease of lactate dehydrogenase (LDH) in cerebrum and improve the learning and memory impairment on the step down test. On the fourvessel occlusion model in rats, Hyp(50 and 100 mg·kg-1, ip) significantly reduced the decreases of glutathione peroxidase(GSHPx), superoxide dismutase(SOD) and LDH activities in the cerebrum. Hyp was also shown to inhibit the increase of nitric oxide (NO) and malondialdehyde (MDA) contents in the cerebrum and promote the recovery of EEG activities. These results suggest that Hyp has protective effect against cerebral ischemiareperfusion injury via attenuating free radical and NO.
出处
《药学学报》
CAS
CSCD
北大核心
1998年第1期14-17,共4页
Acta Pharmaceutica Sinica
基金
安徽医科大学基金
关键词
金丝桃甙
脑缺血
缺血再灌注
保护作用
Hyperin
Cerebral ischemiareperfusion injury
Nitric oxide
Malondialdehyde