β-七叶皂苷钠对大鼠局灶性脑缺血再灌注损伤的保护机制研究  

Protective Mechanism of β-sodium Aescin on Focal Cerebral Ischemia-reperfusion Injury in Rats

作　　者：郭秦乐 霍康[1] 宋银雪[1] 李娜[1] 杜俊凯[1] 许静[1] Guo Qinyue;Huo Kang;Song Yinxue;Li Na;Du Junkai;Xu Jing(The First Affiliated Hospital of Xi’an Jiaotong University,Xi'an,710061)

机构地区：[1]西安交通大学第一附属医院,西安710061

出　　处：《基因组学与应用生物学》2020年第7期3312-3317,共6页Genomics and Applied Biology

基　　金：西安交通大学第一附属医院基金自由探索项目(2019ZYTS-10);西安市科技计划项目(2016048SF/YX04(2));陕西省自然科学基础研究计划项目(2018JM7021)共同资助。

摘　　要：为探究β-七叶皂苷钠对大鼠局灶性脑缺血再灌注损伤的保护作用及可能的机制,本研究构建大鼠局灶性脑缺血再灌注损伤模型,将大鼠分为假手术组(Sham组)、缺血再灌注损伤模型组(I/R组)和β-七叶皂苷钠治疗组(β-SA组)。对各组大鼠脑神经功能损伤进行评分,用TTC法测量脑梗死体积,用TUNEL染色法检测神经元细胞凋亡情况,用ELISA和Western blotting检测脑组织炎症因子TNF-α、IL-1β的表达水平以及凋亡调控基因Bax和Bcl-2的蛋白表达水平。结果显示,与Sham组大鼠相比,I/R组大鼠神经功能缺损明显(p<0.05),梗死体积增加(p<0.05),细胞凋亡增加(p<0.05),TNF-α和IL-1β水平上升(p<0.05),Bcl-2蛋白表达降低(p<0.05),Bax蛋白表达升高(p<0.05);与I/R组大鼠相比,β-SA组大鼠神经功能缺损得到显著改善(p<0.05),梗死体积减小(p<0.05),TNF-α和IL-1β水平降低(p<0.05),Bcl-2蛋白表达升高(p<0.05),Bax蛋白表达降低(p<0.05)。β-七叶皂苷钠可抑制大脑缺血再灌注损伤中的神经功能损伤、脑梗死和细胞凋亡,其机制与抑制脑组织中促炎因子的释放,调节Bax和Bcl-2的表达有关。To investigate the protective effect ofβ-sodium aescin on focal cerebral ischemia-reperfusion injury in rats and its possible mechanism.A rat model with focal cerebral ischemia-reperfusion injury was constructed.The rats were divided into three groups,including:Sham operation group(Sham),ischemia-reperfusion injury model group(I/R)andβ-sodium aescin treatment group(β-SA).The cerebral neurological damage of each group was scored.The volume of cerebral infarction was measured by TTC method.Apoptosis of neurons was detected by TUNEL staining.Expression of TNF-α&IL-1βwere detected by ELISA and Bax&Bcl-2 protein by Western blotting.The result showed that compared with the Sham group,I/R group showed significant neurological deficits(p<0.05),increased infarct size(p<0.05),and increased apoptosis(p<0.05).Besides,in the I/R group,TNF-αand IL-1βlevel increased(p<0.05),the expression of Bcl-2 protein decreased(p<0.05),and the expression of Bax protein increased(p<0.05);Compared with I/R group,neurological deficit inβ-SA group were significantly improved(p<0.05),infarct area decreased(p<0.05),TNF-αand IL-1βlevels decreased(p<0.05),the expression of Bcl-protein increased(p<0.05),and the expression of Bax protein decreased(p<0.05).β-aescinate can inhibit neurological damage,cerebral infarction and apoptosis in cerebral ischemia-reperfusion injury,its mechanism is related to inhibit the release of pro-inflammatory factors and regulate the expression of Bax and Bcl-2 in brain.

关 键 词：Β-七叶皂苷钠 局灶性脑缺血再灌注损伤 保护机制 

分 类 号：R743.33[医药卫生—神经病学与精神病学]