电针对颈上神经节切除脑缺血大鼠海马CGRP、NPY表达的影响

目的：观察电针对颈上神经节切除脑缺血大鼠海马降钙素基因相关肽（calcitonin generelated peptide，CGRP）及神经肽Y（neuropeptide Y，NPY）表达的影响，探讨电针水沟治疗缺血性脑血管疾病的作用机制。方法：将50只SD大鼠随机分为正常组、模型组、电针组、颈上神经节（superiorcervical ganglion，SCG）切除组、SCG切除十电针组，每组10只，采用链霉亲合素-生物素酶复合物法检测各组大鼠海马CGRP和NPY表达。结果：正常大鼠海马CGRP阳性神经细胞数量较少，模型组及SCG切除组CGRP阳性神经细胞数量显著增加；电针组、SCG切除＋电针组大鼠海马CGRP阳性神经细胞数量显著高于正常组、模型组和SCG切除组（P〈0．01）。模型组大鼠海马NPY阳性神经细胞数量较正常组明显增加（P〈0．01），电针组、SCG切除组及SCG切除＋电针组大鼠海马NPY阳性神经细胞数量显著低于模型组（P〈0．01）。结论：SCG对海马NPY表达具有调控作用，电针可通过调节脑缺血大鼠海马神经肽的表达达到抗脑缺血损伤的作用。

Influences of Electroacupuncture on Expression of CGRP and NPY in the Hippocampus of Cerebral Ischemia Rats with Removal of Superior Cervical Ganglion

Objective： To observe the influence of electroacupuneture on the expression of calcitonin gene-related peptide （CGRP） and neuropeptide Y （NPY） in the hippocampus of cerebral ischemia rats with removal of the superior cervical ganglion（SCG）, and explore the mechanism of electroacupuncture at Shuigou acupoint in treating isehemic eerebrovascular disease. Methods： Fifty rats were averagely randomized into normal group, model group, electroaeupuneture group, SCG removal group and electroacupuneture plus SCG removal group. The expression of CGRP and NPY in the rat hippoeampus in each group was assayed by method of streptavidin-biotinidase complex. Results： The expression of CGRP positive neurocytes was few in normal rats. The expression of CGRP positive neurocytes increased in model group and SCG removal group. Compared with that in normal group, model group and SCG removal group, the expression of CGRP neurocytes in electroacupuncture group and.SCG removal plus electroacupuncture group increased significantly （P〈0. 01）. The expression of NPY neurocytes in model group increased significantly （P〈0.01）. The expression of NPY in electroacupuncture group, SCG removal group and SCG removal group, significantly decreased compared with that in normal group （P〈0. 01） . Conclusion： SCG could regulate the expression of NPY in the hippocampus. Electroacupuncture could treat cerebral ischemia injury by reg ulating the expression of neuropeptides in the hippocampus.