黄芪提取物对局灶性脑缺血再灌注损伤模型大鼠行为学及脑组织中NO含量的影响

目的：探讨黄芪提取物对局灶脑缺血再灌注损伤的保护作用及其机制。方法：采用MCAO（大脑中动脉阻塞法）制备局灶性脑缺血动物模型，然后将SD大鼠随机分为假手术组、模型组、黄芪提取物组（AST组，80mg·kg^-1）、尼莫地平组（0．5mg·kg^-1），用药后，观察药物对脑缺血引起的神经功能缺损症状以及脑组织内NO含量的影响。结果：黄芪提取物组不仅能减轻大鼠的神经功能缺损症状；通过治疗后，各治疗组大鼠大脑皮质神经元病变有一定程度的改善。结论：黄芪提取物对脑缺血再灌注损伤有一定保护作用，其作用机制可能与降低NO浓度，达到减少对脑组织的刺激而产生作用。

Protective Effects Mechanism of AST on Changes of Neurological Deficits and Levels of Nitric Oxide （NO~） in Cerebral Ischemia Injury Rats

Objective ： In the present study, we aim to investigate the protective effects of AST on the changes of neuro- logical deficits and the levels of nitric oxide （NO）. Methods： In the present report, rats were randomized into shamopera- tion group, model group, AST group （80 mg ·kg^-1）and nimodipine group （0.5 mg·kg^-1）. By 4 vessel occlusion meth- od, we evaluated the level changes of nerve function and the levels of NO. Results ： After ischemia reperfusion, the model group neurologic deficit score was higher than that of shamoperation group significantly （ P 〈 0.01 ）. In AST group and nimodipine group, the neurologic deficit scores were lower than those in model group （P 〈 0.05, P 〈 0.01 ）. In model group, NO content was increased （P 〈 0.01 ） compared with the shamoperation group. Through treatment, both in AST group and nimodipine group, NO content was decreased （P 〈 0.01, P 〈 0.05 ） compared with the model group. Conclu- sion： AST can prevent and treat the ischemia and reperfusion injury in some degrees.