Cai Ronglin, Hu Ling, Shen Guoming, Yu Qing, Wang Jie, Wu Zijian, Li Meng
Institute of Acupuncture-Moxibustion and Meridian, Anhui University of CM, Hefei 230038, China.
Zhongguo Zhen Jiu. 2017 Feb 12;37(2):157-161. doi: 10.13703/j.0255-2930.2017.02.013.
To explore the partial action mechanism and the myocardial protective effect differences between electroacupuncture (EA) preconditioning at "Neiguan"(PC 6) and "Taiyuan"(LU 9) in rats with acute myocardial ischemia-reperfusion injury.
Ninety-six Wistar rats were randomly assigned into a sham-operation group, a model group, a Neiguan group and a Taiyuan group, 24 rats in each one. The rats in the Neiguan group and Taiyuan group were treated with EA (2 Hz in frequency, 1 mA in intensity) at "Neiguan" (PC 6) and "Taiyuan" (LU 9) respectively, 20 min per treatment, once a day for consecutive 7 days. The rats in the sham-operation group and model group were treated with immobilization for the same time, and no EA was given. The model of myocardial ischemia-reperfusion injury was established in the model group, Neiguan group and Taiyuan group 24 h after the end of EA, while the rats in the sham-operation group were treated with sham operation (no ligation was made during surgery). The myocardial ischemic size, infarction size, activity of protein kinase C (PKC) and expression of aquaporin1 (AQP1) in each group were detected.
Compared with sham-operation group, the myocardial ischemic size, infarction size, AQP1 expression and PKC activity in the model group were significantly increased (all <0.01); compared with the model group and Taiyuan group, the myocardial ischemic size, infarction size, PKC activity and AQP1 expression were significantly decreased in the Neiguan group (<0.01, <0.05). By Pearson correlation analysis, the changes of AQP1 expression were positively correlated with those of PKC activity after EA preconditioning.
EA preconditioning at "Neiguan" (PC 6) could significantly decrease myocardial AQP1 expression and PKC activity in rats with acute myocardial ischemia-reperfusion injuing, but the effect of EA preconditioning at "Taiyuan"(LU 9) is not obvious; its protective effect is likely to be achieved by inhibiting PKC activity and AQP1 expression.
探讨电针“内关”（PC 6）与“太渊”（LU 9）预处理对急性心肌缺血再灌注损伤大鼠的部分作用机制及心肌保护作用差异。
将96只Wistar大鼠随机分为假手术组、模型组、内关组和太渊组，每组24只。内关组和太渊组大鼠分别于“内关”（PC 6）和“太渊”（LU 9）进行电针治疗（频率2 Hz，强度1 mA），每次治疗20 min，每天1次，连续7天。假手术组和模型组大鼠进行相同时间的固定，不给予电针治疗。电针结束24 h后，模型组、内关组和太渊组建立心肌缺血再灌注损伤模型，假手术组大鼠进行假手术（手术过程中不结扎）。检测各组心肌缺血面积、梗死面积、蛋白激酶C（PKC）活性及水通道蛋白1（AQP1）表达。
与假手术组比较，模型组心肌缺血面积、梗死面积、AQP1表达及PKC活性显著增加（均P<0.01）；与模型组和太渊组比较，内关组心肌缺血面积、梗死面积、PKC活性及AQP1表达显著降低（P<0.01，P<0.05）。经Pearson相关性分析，电针预处理后AQP1表达变化与PKC活性变化呈正相关。
电针“内关”（PC 6）预处理可显著降低急性心肌缺血再灌注损伤大鼠心肌AQP1表达及PKC活性，但电针“太渊”（LU 9）预处理效果不明显；其保护作用可能是通过抑制PKC活性及AQP1表达实现的。
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