摘要
目的:探讨邓铁涛教授健脑1方对血管性痴呆大鼠的海马NMDAR-CaMKⅡ通路的影响。方法:采用双侧颈总动脉永久性结扎建立VD动物模型,将60只SD雄性大鼠随机分为假手术组、VD模型组、高剂量组、低剂量组及尼莫地平组,给药30天后采用免疫组化方法测定大鼠海马CAl区NR2B及CaMKⅡ表达水平。结果:模型组大鼠海马CAl区NR2B及CaMKⅡ的表达水平与假手术组相比明显降低(P<0.01)。与模型组相比较,高剂量组大鼠海马CAl区NR2B及CaMKⅡ表达水平均显著提高(P<0.05),尼莫地平组大鼠海马CAl区CaMKⅡ表达水平也明显提高(P<0.05)。结论:NMDAR-CaMKⅡ通路在VD的发生机制中发挥了重要作用。健脑1方可能通过上调VD大鼠海马NR2B及CaMKⅡ的表达,从而改善大鼠学习和记忆功能,起到治疗血管性痴呆的作用。
Objective ：To observe effect of Professor DENG Tietao＇s Brain - strengthening Recipe Ⅰ on NMDAR - CaMK Ⅱ Pathways in hippocampus of rats with vascular dementia. Methods ： The vascular dementia rat model was established by permanent bilateral occlusion of the common carotid arteries. Sixty male SD rats were randomly divided into 5 groups： sham - operated group, VD model group, high dosage group, low dosage group and nimodipine group. After 30 days of medicatin, the expressions of NR2B and CaMK Ⅱ in the hippocampal CA1 region in rats were measured by immunohistochemical techniques techniques. Results ： The expressions of NR2B and CaMK Ⅱ were significantly decreased in the hippocampal CAI region in rats of the model group than that of the sham - operated group （ P 〈 0. 01 ）. Compared with the model group, the expressions of NR2B and CaMK Ⅱ were siginificantly increased in the hippocampal CA1 region in rats of the high dosage group （P 〈0. 05）. The expression of CaMK Ⅱ was also increased in nimodipine group（ P 〈 0. 05 ）. Conclusions ： NMDAR - CaMK Ⅱ pathway plays an important role in the pathogenesis of VD. Brain - strengthening Recipe 1 can up - regulate the expressions of NR2B and CaMK Ⅱ in the hippocampus of rats, thus improving learning and memorizing abilities of VD rats.
出处
《中华中医药学刊》
CAS
北大核心
2017年第3期639-641,I0017,I0018,共5页
Chinese Archives of Traditional Chinese Medicine
基金
广东省科技厅项目(2014A020221018)
