电针对脑缺血大鼠缺血皮质区内皮型一氧化氮合酶及血清中一氧化氮含量的影响

目的 观察电针对大脑中动脉缺血大鼠缺血皮质区内皮型一氧化氮合酶（endothelial nitric oxide synthase，eNOS）及一氧化氮（nitric oxide，NO）的调控作用。方法 取SPF级健康雄性大鼠随机分为假手术组、模型组、电针组，每组14只，利用改良线栓法制备脑缺血大鼠模型，电针组选取“百会”“风府”“内关”“心俞”4个穴位，从第1天术后4 h开始治疗，每日1次，共治疗7 d。干预结束后，比较各组大鼠神经功能评分、脑梗死体积、脑缺血皮质区细胞病理表现、缺血皮质区eNOS蛋白的表达、血清NO的含量。结果 与假手术组比较，模型组大鼠神经功能缺损体征明显（P<0.05），梗死范围显著，脑缺血皮质区eNOS蛋白表达显著下降（P<0.05），血清NO含量升高（P<0.05）；与模型组比较，电针组大鼠神经功能缺损评分降低（P<0.05），脑梗死体积明显缩小（P<0.05），脑皮质缺血区eNOS蛋白表达水平显著上升（P<0.05），血清NO含量升高（P<0.05）。结论 电针可促进局灶性脑缺血大鼠神经功能的恢复并缩小脑梗死体积，其机制可能与调控血管新生相关因子eNOS、NO表达增多有关。

Effect of Electroacupuncture on the Expression of Endothelial Nitric Oxide Synthase in the Ischemic Cortex and the Serum Level of Nitric Oxide in Rats with Cerebral Ischemia

Objective To investigate the regulatory effect of electroacupuncture (EA) on the expression of endothelial nitric oxide synthase (eNOS) in the ischemic cortex and the serum level of nitric oxide (NO) in rats with cerebral ischemia. Methods Specific pathogen-free healthy male rats were randomly divided into sham-operation group, model group, and EA group, with 14 rats in each group. The modified suture method was used to establish a rat model of cerebral ischemia. The rats in the EA group were treated by EA at Baihui, Fengfu, Neiguan, and Xinshu since day 1 at 4 hours after surgery, once a day for 7 days. After intervention, the three groups were compared in terms of neurological score, cerebral infarct volume, pathological manifestations of the cells in the ischemic cortex, protein expression of eNOS in the ischemic cortex, and serum level of NO. Results Compared with the sham-operation group, the model group had obvious signs of neurological defects (P<0.05), a significant increase in infarct volume, a significant reduction in the protein expression of eNOS in the ischemic cortex (P<0.05), and a significant increase in the serum level of NO (P<0.05). Compared with the model group, the EA group had significant reductions in neurological deficit score and cerebral infarct volume (P<0.05) and significant increases in the protein expression of eNOS in the ischemic cortex and the serum level of NO (P<0.05). Conclusion EA can promote the recovery of neurological function and reduce infarct volume in rats with cerebral ischemia, possibly by upregulating the expression of the angiogenesis-related factors eNOS and NO.