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黄芪甲苷对大鼠脑缺血再灌注损伤的保护作用和机制研究

The Protective Effect and Mechanism of Astragaloside in Cerebral Ischemia Reperfusion in Rats

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【作者】 孙丽王岭李艳张进房雷

【Author】 SUN Li;WANG Ling;LI Yan;ZHANG Jin;FANG Lei;Department of Neurology, the Central Hospital of Qingdao City;

【机构】 青岛市中心医院神经科

【摘要】 目的探讨黄芪甲苷对大鼠脑缺血/再灌注损伤的神经保护作用和机制。方法应用线栓法建立大鼠大脑中动脉阻塞再灌注模型(模型组),建模成功大鼠经腹腔注射黄芪注射液(每毫升含黄芪甲苷1 mg)干预治疗(黄芪治疗组,再随机分为黄芪低剂量组、中剂量组和高剂量组)。另设对照组(插线进入大鼠颈内动脉10 mm后即刻退出)。Longa法评价大鼠神经行为功能,苏木精-伊红染色观察大鼠皮质区神经元形态结构,TUNEL检测细胞凋亡,免疫组化检测脑源性神经营养因子(BDNF)、血管内皮生长因子(VEGF)及血管内皮生长因子受体2(VEGFR2)蛋白表达。结果经黄芪注射液治疗后,大鼠脑组织BDNF、VEGF、VEGFR2蛋白表达较对照组显著增加,且BDNF主要在海马区表达,VEGF及VEGFR2主要在皮质区表达,脑组织凋亡细胞数量显著减少,大鼠神经行为功能显著改善。结论黄芪注射液可通过增加BDNF、VEGF及VEGFR2的表达而抑制细胞凋亡,刺激神经再生,促进受损神经的修复,改善大鼠的神经行为功能,黄芪中剂量和高剂量作用更为明显。

【Abstract】 Aim To study the protective effect and mechanism of astragaloside in cerebral ischemia reperfusion in rats. Methods The middle cerebral artery occlusion reperfusion(MCAO/R) rat models were established by inserting a filament suture from left external-internal carotid artery, and treated by injecting intraperitoneally astragalus injection. The rat neurobehavioral function was evaluated by Longa’s test, hematoxylin eosin(HE) staining was used to observe the morphological structure of cortical neurons, apoptosis was detected by TUNEL and the expressions of brain derived neurotrophic factor(BDNF), vascular endothelial growth factor(VEGF) and its receptor(VEGFR2) protein were detected by immunohistochemistry. Results After the treatment with astragalus injection, the expression of BDNF, VEGF and its receptor VEGFR2 protein in rats brain increased significantly compared with the control group, and BDNF mainly expressed in hippocampus, VEGF and its receptor VEGFR2 mainly expressed in cortex. The number of apoptotic cells in brain tissue significantly reduced, while the animal neurobehavioral function improved significantly. Conclusion Astragalus injection can inhibit apoptosis, stimulate the nerve regeneration, promote the nerve repairment and improve the nerve behavior function in animal by increasing the expression of BDNF, VEGF and its receptor VEGFR2.

【基金】 山东省医药卫生科技发展计划(编号:2011HW034)
  • 【文献出处】 中国临床神经科学 ,Chinese Journal of Clinical Neurosciences , 编辑部邮箱 ,2014年01期
  • 【分类号】R285.5
  • 【被引频次】36
  • 【下载频次】419
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