摘要
【目的】探讨黄芪甲甙对局灶性脑缺血的保护作用及其可能的机制。【方法】40只雄性SD大鼠随机分为4组:假手术组、模型组、低剂量干预组(10mg/kg.d)和高剂量干预组[20 mg/(kg.d)],每组10只。采用大脑中动脉阻塞(MACO)法制备大鼠局灶性脑缺血模型,术后24h观察神经行为学变化并评分,然后处死动物并测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH)活性和丙二醛(MDA)含量,脑梗死区重量用TTC染色法测定,用原位末端标记法(TUNEL)检测脑组织细胞凋亡指数(AI)。【结果】与模型组比较,低、高剂量干预组神经学评分和脑梗死组织重量明显降低,差异有显著性(P<0.05或0.01)。低、高剂量干预组脑组织SOD、GSH活性增加,MDA含量及AI降低,与模型组相比,差异均有显著性(P<0.05或0.01)。【结论】黄芪甲甙对大鼠局灶性脑缺血有明显的保护作用,其机制可能与抗自由基及抑制细胞凋亡有关。
[Objective]To explore the protective effect of astragaloside on local cerebral ischemia in rats and its mechanism involved. [Methods] Forty male SD mice were randomly divided into 4 groups： false operation group, model group, low-dose intervention group （10mg/kg · d ） and high-dose intervention group （20mg/kg · d）. There were 10 rats in every group. The local cerebral ischemia in rats was made by middle cerebral artery occlusion （MACO）. The neurological outcome of each group was evaluated at 24h after operation. Then all rats were killed, and SOD, GSH and MDA were measured. The infraction weight was determined by TTC stain. Apoptosis index （AI） was measured by biotinyated -dUTP nick and labeling （TUNEL）. [Resuits] The neurologic deficit scores and infraction weight were markedly lower in low and high-dose interven tion groups than those in model group （ P 〈0.05 or 0.01）. SOD and GSH were significantly increased in low and high-dose intervention groups than those in model group （ P 〈0.05 or 0.01）. MDA and AI were decreased in low and high-dose groups compared with model group （ P 〈0.05 or 0.01）. [Conclusion] Astragaloside has obvious protective effect against cerebral ischemia in rats, and its mechanism may be related to antifree radicals and the inhibition of cell apoptosis.
出处
《医学临床研究》
CAS
2008年第5期814-816,共3页
Journal of Clinical Research
关键词
脑缺血/药物疗法
黄芪
皂苷类
Brain isehemia/DT
astragalus membranaeeus
saponins
