黑木耳多糖对急性脑缺血/再灌注损伤影响的研究

Study of the effects of Auricularia Auricular polysaccharide on local ischemia/reperfusion injury in rat

目的:观察黑木耳多糖(APP)对急性脑缺血大鼠的保护作用并探讨其相关机制。方法:成年雄性SD大鼠给予不同浓度的AAP灌胃20d,每天1次,腹腔注射银杏叶提取物(ginkgo biloba extract,EGb671)作为阳性对照,20d后实施右侧大脑中动脉栓塞(MCAO)建立局灶性脑缺血模型。MCAO60min后复灌,复灌24h后进行Longa神经功能损伤评分,并用2,3,5-氯化三苯基四氮唑(TTC)染色法测定脑梗死面积。复灌48h后用TUNEL免疫组化检测神经元凋亡,测定脑组织线粒体内活性氧簇(ROS)的生成量判断氧化应激水平。结果:黑木耳多糖能降低神经功能损伤评分,减小脑梗死面积,减少神经元凋亡,并且能够使缺血复灌脑组织线粒体ROS生成显著减少。高剂量AAP组的凋亡神经元数量、ROS生成量和阳性对照组相比有显著性差异。结论:黑木耳多糖能够对抗大鼠的局灶性脑缺血损伤,其保护作用和减轻氧化应激水平有关,并优于银杏叶提取物。

Objective：To investigate the influence of Auricularia Auricular polysaccharide （APP） on acute cerebral injury induced by ischemia/reperfusion in rats and its underlying mechanism. Methods： Adult male SD rats were intragastrically pretreated with AAP at a low （50 mg/kg） or high （100 mg/kg） dose once a day for 20 days before operation. Rats intraperitonealy injected with ginkgo biloba extract （EGb671） were taken as positive control. Focal ischemia was achieved by middle cerebral artery occlusion （MCAO） on the right side for 60 min. After 24 hrs of reperfusion,the nerve function defects were recorded by Longa’s score and the brain infarct sizes were measured by 2,3,5-Triphenyltetrazoliumchlor （TTC） staining. Apoptotic neurons were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） staining after 48 h of reperfusion. The levels of oxidative stress was determined via the mitochondria-generated reactive oxygen species （ROS）. Results： AAP treatment decreased Longa’s score,brain infart size,apoptotic neurons and mitochondria-generated ROS in a dose-dependent manner. AAP at 100 mg/kg gave a better performance compared with EGb671 on all parameters examined. Conclusion： AAP treatment protected rat brain from focal ischemia/reperfusion injury by its anti-oxidative effect and worked better than EGb671.