电针对局灶性脑缺血大鼠缺血皮质区内皮抑素、血小板反应蛋白-1表达的影响
Effect of Electroacupuncture on the Expression of Endostatin and Thrombospondin-1 in the Ischemic Cortex in Rats with Focal Cerebral Ischemia
  
DOI:
中文关键词:  电针  脑缺血  内皮抑素  血小板反应蛋白-1
英文关键词:Electroacupuncture  Focal cerebral ischemia  Endostatin  Thrombospondin-1
基金项目:国家自然科学基金项目(81373711,81874500);安徽高校科研创新平台团队建设项目(2015TD033);第九批安徽省学术和技术带头人后备人选项目(2013025)
作者单位
李斯亮,唐 巍,龚 丽,昝兴淳,丰丽媛,童明月,何 鹏 1.安徽中医药大学研究生院安徽 合肥 2300122.安徽中医药大学针灸推拿学院安徽 合肥 230012 
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中文摘要:
      目的 观察电针对局灶性脑缺血大鼠缺血皮质区内皮抑素(endostatin,ES)、血小板反应蛋白-1(thrombospondin-1,TSP-1)表达的调控作用及其机制。方法 将54只健康雄性SD大鼠随机分为假手术组、模型组和电针组,每组18只。利用改良线栓法复制局灶性大脑中动脉闭塞模型,电针组选取“百会”与“水沟”穴进行治疗,每次30 min,每日1次,共干预7 d。比较术后7 d各组大鼠神经功能评分,用2,3,5-三苯基氯化四氮唑染色法测量脑梗死面积,免疫组织化学法及蛋白免疫印迹法检测ES、TSP-1蛋白在大鼠脑缺血皮质区的表达情况。结果 与假手术组比较,模型组大鼠神经功能缺损体征较为显著,梗死范围明显,脑缺血皮质区ES和TSP-1蛋白表达均显著上调(P<0.05);与模型组比较,电针组大鼠神经功能评分降低(P<0.05),梗死面积缩小(P<0.05),脑缺血皮质区ES、TSP-1蛋白表达水平均明显下调(P<0.05)。结论 电针可促进局灶性脑缺血大鼠神经功能恢复,缩小梗死面积,其机制可能与血管新生抑制因子ES、TSP-1的表达下调有关。
英文摘要:
      Objective To observe the effect of electroacupuncture(EA) on the expression of endostatin (ES) and thrombospondin-1 (TSP-1) in the ischemic cortex in rats with focal cerebral ischemia(FCI) and its mechanism.Methods Fifty-four healthy male Sprague-Dawley rats were randomly divided into sham-operation group,model group, and EA group, with 18 rats in each group. A right middle cerebral artery occlusion model was established by the modified suture method. The EA group was treated by EA (30 min) at Baihui and Shuigou points once daily for 7 days. The neurological score was assessed at 7 d after operation.The cerebral infarct area was measured by 2,3,5-triphenyltetrazolium chloride staining. Immunohistochemistry and Western blot were used to measure the protein expression of ES and TSP-1 in the ischemic cortex. Results Compared with the sham-operation group,the model group showed obvious signs of neurological deficit, with a significantly increased neurological score,an obvious infarct area, and significantly upregulated protein expression of ES and TSP-1 in the ischemic cortex (P<0.05). Compared with the model group,the EA group had a significantly lower neurological score(P<0.05), a significantly smaller infarct area(P<0.05), and significantly downregulated expression of ES and TSP-1 in the ischemic cortex(P<0.05). Conclusion EA can promote neurological recovery and reduce the infarct area in rats with FCI, possibly by down-regulating the expression of angiogenesis inhibitors ES and TSP-1.
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