电针“心俞-神门”对急性心肌缺血模型大鼠心肌与海马组织Glu、Asp和NR1表达的影响

Effects of Electroacupuncture at"Xinshu(BL15)-Shenmen(HT7)"on the Expression of Glu,Asp and NR1 in the Myocardial and Hippocampal Tissues of Acute Myocardial Ischemia Rat

目的观察电针“心俞-神门”配穴对急性心肌缺血(acute myocardial ischemia,AMI)模型大鼠心肌和海马组织谷氨酸(Glu)、天冬氨酸(Asp)和N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体亚基NMDAR1(NR1)的影响,探讨俞原配穴的协同效应,及其对AMI致脑损伤保护的作用机制。方法将60只健康雄性SD大鼠随机分为假手术组、模型组、电针“神门”组(神门组)、电针“心俞”组(心俞组)和电针“心俞+神门”组(心神组),每组12只。除假手术组外,其他4组大鼠选用冠状动脉左前降支结扎法建立AMI模型。干预组每天电针治疗1次,20 min/次,共治疗1周,假手术组和模型组不作干预治疗。观察分析心电图ST段变化;ELISA法检测各组大鼠心肌和海马组织中Glu、Asp浓度;实时荧光定量PCR检测各组大鼠心肌和海马组织中NR1 mRNA表达。结果与假手术组比较,模型组大鼠心电图ST段明显抬高(P<0.01),心肌、海马Glu、Asp浓度和NR1 mRNA表达均显著上升(P<0.01);与模型组比较,3组电针组治疗后ST段明显降低(P<0.01),心神组心肌和海马Glu、Asp浓度、NR1 mRNA表达均明显下降(P<0.01),神门组、心俞组心肌和海马NR1 mRNA表达及心肌Asp、海马Glu浓度均显著下降(P<0.01);与神门组比较,心神组心肌Asp浓度和海马Glu、Asp浓度及心肌和海马的NR1 mRNA表达均明显下降(P<0.05或P<0.01);与心俞组比较,心神组心肌和海马Asp浓度、NR1 mRNA表达明显下降(P<0.05或P<0.01)。Pearson相关分析显示,电针治疗后心肌、海马组织中Glu浓度与NR1 mRNA表达呈正相关。结论电针俞原配穴“心俞-神门”能够改善AMI模型大鼠心肌缺血状态,降低心肌组织和海马组织的兴奋性氨基酸Glu、Asp和NR1水平,可能是其发挥保护心肌缺血致脑损伤的作用机制之一。

Objective To observe the effect of electroacupuncture at“Xinshu(BL15)-Shenmen(HT7)”acupoint matching on the glutamic acid(Glu),aspartic acid(Asp)and the N-methyl-D-aspartate(NMDA)receptor subunit NMDAR1(NR1)in myocardial and hippocampal tissues of acute myocardial ischemia(AMI)model rats,in order to explore the synergistic effect of acupoint matching of shu-point and source-point and their mechanism in protecting brain injury caused by AMI.Methods 60 healthy male SD rats were randomly divided into the sham operation group,the model group,the electroacupuncture at“Shenmen(HT7)”group(HT7 group),the electroacupuncture at “Xinshu (BL15)” group (BL15 group), and the electroacupuncture at "Xinshu (BL15)-Shenmen (HT7)" group (BL15-HT7 group), with 12 in each group. The AMI model was established by ligation of left anterior descending coronary artery in four groups except the sham operation group. Each intervention group received electroacupuncture treatment once a day for 20 minutes each time for 1 week. The sham operation group and the model group did not receive intervention treatment. The electrocardiogram of rats were recorded, and the changes of ST segment were observed and analyzed;the concentration of Glu and Asp in rat myocardial and hippocampal tissues were determined by ELISA;quantitative realtime PCR was used to detect the expression of NR1 mRNA in the myocardial and hippocamal tissues of rats in each group. Results Compared with the sham operation group, the ST segment of the model group was significantly elevated (P<0.01), the concentration of Glu and Asp, and the expression of NR1 mRNA in myocardial and hippocamal tissues were significantly increased (P<0.01);compared with the model group, the ST segment of three groups of electroacupunture were obviously decreased after treatment (P<0.01), the concentration of Glu, Asp and the expression of NR1 mRNA in myocardial and hippocamal tissues were decreased significantly in the BL15-HT7 group (P<0.01), the expression of NR1 mRNA in myocardial and hippocamal tissues, the myocardial Asp and the hippocampal Glu concentration were significantly decreased in the HT7 group and the BL15 group (P<0.01);compared with the HT7 group, the concentration of myocardial Asp and hippocampal Glu, Asp, and the expression of NR1 mRNA in myocardial and hippocamal tissues were decreased significantly in BL15-HT7 group (P<0.05 or P<0.01);compared with BL15 group, the concentration of myocardial and hippocampal Asp and the expression of NR1 mRNA were significantly decreased in BL15-HT7 group (P<0.05 or P<0.01). Pearson correlation analysis showed that the concentration of Glu myocardial and hippocamal tissues were positively correlated with the expression of NR1 mRNA after electroacupuncture. Conclusion Electroacupuncture acupoint matching of shu-point and source-point of "Xinshu (BL15)-Shenmen (HT7)" can improvemyocardial ischemia in AMI rats and reduce the concentration of excitatory amino acid Glu and Asp, and the NR1 expression in myocardial and hippocampal tissues, which may be one of the mechanisms of protecting brain damage caused by myocardial ischemia.