Zhang Qian, Zhang Chuang, Zhang Jia-Yin, Zhang Hui-Zhen, Li Xiao-Feng, Xiao Hong-Ling, Sun Yan-Hui, Xing Hai-Jiao, Xu Xiao-Kang, Liang Yu-Lei, Zhang Xin, Zhang Xiao-Qi, Li Ai-Ying
College of Traditional Chinese Medicine, Hebei Medical University, Shijiazhuang 050091, China.
The Scientific Research Center of Hebei College of Traditional Chinese Medicine, Shijiazhuang 050091.
Zhen Ci Yan Jiu. 2016 Dec 25;41(6):509-14.
To observe the influence of electroacupuncture (EA) intervention on hippocampal glutamate (Glu) and Ca contents, and expression of Glu-N-methyl-D-aspartic acid receptor(NMDAR) and the learning-memory ability in vascular dementia (VD) rats, so as to reveal its mechanisms underlying improvement of VD.
SD rats were rando-mized into sham operation (sham) group (=9), model group (=11) and EA groups (=10). The VD model was established by repeated bilateral common carotid arteries occlusion and reperfusion plus intraperitoneal injection of sodium nitroprusside. EA (2 Hz, 2 mA) was applied to "Baihui" (GV 20)-"Housanli" (ST 36) and "Geshu" (BL 17)-"Dazhui" (GV 14) for 10 min, once a day for 15 consecutive days. The neurological function was assessed by using stroke index (0-10 points) and neurological deficit scaling(0-10 points). The learning-memory ability was evaluated by using step-down tests. The contents of Glu and Ca in the right hippocampal tissue were determined by using aspectrophotometer and the expression of NMDAR protein in the right hippocampus was detected by immunoblotting.
Compared with the sham group, the stroke index and neurological deficit scores, and the reaction latency and the error times of step-down tests, as well as the contents of Glu and Ca and the expression level of NMDAR in the right hippocampus were significantly increased in the model group (<0.05, <0.01), while the step-through latency was considerably decreased (<0.01), suggesting a neurological disorder and a cognitive decline. After EA intervention, the reaction latency and error times of step-down tests, the contents of Glu and Ca and the expression level of NMDAR in the right hippocampus were significantly down-regulated, and the step-through latency was notably increased in comparison with the model group (<0.01).
EA intervention is able to improve the cognitive ability of VD rats, which may be associated with its effects in reducing the excitatory neurotoxicity of hippocampal Glu-NMDAR and lowering cellular Ca load to resist neuronal injury.
观察电针干预对血管性痴呆（VD）大鼠海马谷氨酸（Glu）、钙含量、Glu-N-甲基-D-天冬氨酸受体（NMDAR）表达及学习记忆能力的影响，以揭示其改善VD的作用机制。
将SD大鼠随机分为假手术组（n = 9）、模型组（n = 11）和电针组（n = 10）。采用双侧颈总动脉反复夹闭再灌注并腹腔注射硝普钠的方法建立VD模型。电针（2 Hz，2 mA）刺激“百会”（GV 20）-“后三里”（ST 36）及“膈俞”（BL 17）-“大椎”（GV 14），每次10分钟，每日1次，连续15天。采用卒中指数（0 - 10分）和神经功能缺损评分（0 - 10分）评估神经功能。采用跳台试验评估学习记忆能力。用分光光度计测定右侧海马组织中Glu和钙的含量，用免疫印迹法检测右侧海马中NMDAR蛋白的表达。
与假手术组比较，模型组卒中指数、神经功能缺损评分、跳台试验反应潜伏期和错误次数以及右侧海马Glu、钙含量和NMDAR表达水平均显著升高（P < 0.05，P < 0.01），而穿通潜伏期显著缩短（P < ），提示存在神经功能障碍和认知功能下降。电针干预后，与模型组比较，跳台试验反应潜伏期和错误次数、右侧海马Glu和钙含量以及NMDAR表达水平均显著下调，穿通潜伏期显著延长（P < 0.01）。
电针干预可提高VD大鼠的认知能力，其机制可能与降低海马Glu-NMDAR兴奋性神经毒性、降低细胞钙负荷以抵抗神经元损伤有关。
