冠元颗粒增强局灶性脑缺血耐受的作用机制研究

Study of the action mechanisms of Guan-yuan granula on enhancement of focal cerebral ischemia tolerance

目的探讨冠元颗粒对局灶性脑缺血耐受的影响及其作用机制。方法30只SD大鼠随机分为3组,模型组10只予单纯预缺血+缺血(IPC+MCAO),给药组10只予预缺血+冠元颗粒+缺血(IPC+GY+MCAO)处理,假手术组以假手术代替预缺血,余同模型组。利用线栓法建立局灶性脑缺血耐受的动物模型。比较各组神经功能评分、组织病理改变及脑源性神经营养因子(BDNF)表达的变化。结果局灶性缺血预处理能够有效促进大鼠的神经行为功能的恢复,减轻组织学的损伤,增加BDNF表达,其中给药组病理改变最轻,其BDNF水平较模型组有显著性差异(P<0.05)。结论局灶性缺血预处理对随后的脑梗死有明显的保护作用,能够诱导缺血耐受的产生,其可能的机制之一是上调BDNF的表达;冠元颗粒能够进一步诱导其表达的上调,增强其对神经元的保护作用,减轻再次缺血的损伤。

Objective It is to approach the influence and action mechanisms of Guan-yuan granula on focal cerebral ischemia tolerance. Methods 30 SD rats were divided into 3 groups： model group （n = 10） with ischemic preconditioning （IPC） ＋ ischemia （MCAO）, administration group （n= 10） with IPC ＋ Guan-yuan granula （GY） ＋ MCAO and notho- operation group （n= 10） with notho-operation ＋ MCAO. The model of focal cerebral ischemia tolerance was made by the method of bind. The changes of histological and the expression of brain-derived neurotrophic factor （BDNF） were evaluated. Results Focal cerebral ischemic preconditioning can significantly reduce the following infarct volume and the damage of histology and up-regulate the expression of BDNF. And the effection in the administration group is especially more obvious than the others （P〈0.05）. Conclusion Focal cerebral ischemic preconditioning can provide brain and induce ischemic tolerance. Up-regulation of the expression of BDNF might play an important mechanism. And Guan-yuan granula can induce the upregulation of the expression of BDNF, and enhance neurone protection, reduce the second ischemic injure.