Liu Chun-Li, Chen Hong, Jiang Yong, Tu Peng-Fei, Zhong Ming, Ma Jing-Yi, Ding Hui, Zhang Wan-Xin, Jin Xiao-Min
Key Laboratory of Xinjiang Endemic Phytomedicine Resources of Ministry of Education, School of Pharmacy, Shihezi University, Shihezi 832002, China.
Yao Xue Xue Bao. 2013 May;48(5):790-3.
The aim of this study is to investigate the effect of echinacoside (ECH) on cholinergic neurotransmitter extracellular of hippocampus and striatum and its possible mechanisms of neuro-protective effect against vascular dementia rats. In this study brain microdialysis technique combined with HPLC-IMER-ECD (high-performance liquid chromatography-immobilized enzyme reactor-electrochemical detector) was used. The bilateral common carotid arteries occluded in two times operation at 72 h interval for vascular dementia model rats were used and the successful vascular dementia model rats were examined by Morris water maze. The content of acetylcholine (ACh) and choline (Ch) of microdialysate extracellular of hippocampus and striatum was determined by HPLC-IMER-ECD and the AChE activity in the hippocampus was measured. The results showed that the success rate of vascular dementia model was 83.08% after six weeks; the results also showed that echinacoside and galantamine could increase the content of ACh and reduce the content of Ch extracellular of hippocampus and striatum significantly and the AChE activity increased significantly compared with that of the model group. The results suggested that echinacoside could promote the recovery of cholinergic neurotransmitter levels in vascular dementia rats' brain, which may be one of the mechanisms of neuro-protection.
本研究旨在探讨紫锥菊苷(ECH)对海马和纹状体胆碱能神经递质细胞外水平的影响及其对血管性痴呆大鼠神经保护作用的可能机制。本研究采用脑微透析技术结合高效液相色谱-固定化酶反应器-电化学检测器(HPLC-IMER-ECD)。采用间隔72小时两次手术阻断双侧颈总动脉的方法制备血管性痴呆模型大鼠,并通过Morris水迷宫对成功的血管性痴呆模型大鼠进行检测。采用HPLC-IMER-ECD测定海马和纹状体细胞外微透析液中乙酰胆碱(ACh)和胆碱(Ch)的含量,并检测海马中乙酰胆碱酯酶(AChE)的活性。结果显示,六周后血管性痴呆模型成功率为83.08%;结果还表明,紫锥菊苷和加兰他敏可显著增加海马和纹状体细胞外ACh含量,降低Ch含量,且与模型组相比,AChE活性显著升高。结果提示,紫锥菊苷可促进血管性痴呆大鼠脑内胆碱能神经递质水平的恢复,这可能是其神经保护机制之一。