黄芪提取物对局灶性脑缺血再灌注损伤的抗氧化及线粒体保护作用

Anti-oxidative and mitochondria-protective effects of extract of astragalus on focal cerebral ischemia-reperfusion injury in rats

目的 研究黄芪提取物 (Extractofastragalus,EA)对局灶性脑缺血再灌注损伤大鼠的抗氧化及线粒体保护作用。方法 采用栓线法复制局灶性脑缺血 (MCAO)再灌注损伤模型,观察EA对大鼠脑组织匀浆中超氧化物歧化酶(SOD)、丙二醛(MDA)和乳酸 (LD)的影响;检测脑组织线粒体组分中的SOD、MDA含量及ATP酶活性的变化 ;电镜观察缺血再灌注后脑组织神经元超微结构的改变。结果 EA对大鼠MCAO2h再灌注 24h后脑组织及其线粒体组分中SOD活性的降低有明显的抑制作用,能抑制大鼠脑组织和脑组织线粒体组分中MDA含量的增加,能抑制大鼠脑组织LD含量的增加; EA可明显提高脑组织线粒体组分中Na+,K+ ATPase,Ca2+,Mg2+ ATPase活性;电镜照片显示EA组能改善脑组织神经元在脑缺血再灌注后的结构破坏情况。结论 EA对局灶性脑缺血再灌注损伤大鼠的保护作用的机制可能与其抗脂质过氧化和保护线粒体的作用有关。

Aim To study the anti-oxidative and mitochondria-protective effects of estract of astragalus (EA ) on focal cerebral ischemia-reperfusion injury and its mechanism in rats.Methods Middle cerebral artery occlusion(MACO) was used to induce focal cerebral ischemia-reperfusion model. After 24 h reperfusion,MDA, LD content and SOD activity of brain homogenate were tested. MDA content,SOD and ATPase activity in mitochondrion were also tested.Transmission electron microscopy was used to assess the ultrastructure dstruction. Results EA(20, 40, 80 mg·kg -1) significantly inhibited the increase of MDA, LD after cerebral ischemia-reperfusion. EA (40, 80 mg·kg -1) also inhibited the decrease of activit of SOD in rats. EA(20, 40, 80 mg·kg -1) inhibited the increase of MDA and inhibited the decrease of activities of SOD, Na+,K+-ATPase, Ca 2+,Mg 2+-ATPase in mitochondrion. The examination by transmission electron microscopy showed that EA (20, 40 mg·kg -1) protected the ultrastructure destruction. Conclusion EA had protective effects against focal cerebral ischemia reperfusion injuries via attenuating cerebral oxygen free radical(OFR)lipid peroxidation and protecting mitochondria.