Zhu Yi, Li Yi, Zhang Nan, Dong Gui-Rong
Department of Acupuncture-moxibustion, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, China.
Zhen Ci Yan Jiu. 2018 May 25;43(5):302-6. doi: 10.13702/j.1000-0607.170308.
To observe the effect of electroacupuncture (EA) preconditioning on acute myocardial ischemia (MI) and expression of Toll-like receptor 4 (TLR 4), myeloid differentiation factor 88 (MyD 88) and nuclear factor-κB (NF-κB) mRNAs in the "Neiguan" (PC 6) area of rats with MI-reperfusion injury (MIRI), so as to explore its mechanisms underlying improvement of MIRI.
Forty-eight male Wistar rats were randomly divided into control, control ＋ EA, sham operation, model, EA and sham EA groups (＝8). The MIRI model was established by occlusion of the descending anterior branch of the left coronary artery for 30 min, followed by reperfusion. Before modeling, EA preconditioning was respectively applied to PC 6 or sham PC 6 for 30 min, once daily for 5 days. Electrocardiogram (ECG) of the standard limb-lead Ⅱ was recorded before and after the modeling, and 0.25 h after reperfusion. The expression levels of TLR 4, MyD 88 and NF-κB genes in the PC 6 tissue were detected by Real-time PCR.
Compared with the control group, the height of ECG J-point was significantly increased in the model group (<0.01), suggesting an acute MI, and the height of J-point was significantly lower in the EA group than in the model and sham EA groups (<0.01). In comparison with the control group, the expression levels of TLR 4, MyD 88 and NF-κB mRNAs were markedly up-regulated in the area of PC 6 in the model group (<0.01). Compared with the model group, the increased expression levels of TLR 4, MyD 88 and NF-κB mRNAs in the EA preconditioning group were significantly inhibited (<0.05). No significant differences were found among the control, control＋EA and sham operation groups and between the model and sham EA groups in the expression levels of TLR 4, MyD 88 and NF-κB mRNAs (>0.05)．.
EA preconditioning can improve myocardial ischemia and reduce the expression of TLR 4, MyD 88 and NF-κB mRNAs in PC 6 area of MIRI rats, suggesting an involvement of the regional cutaneous TLR 4/MyD 88/NF-κB signaling suppression in the initiation-transfer-amplification of EA stimulating signal inputs for relieving MIRI.
观察电针预处理对心肌缺血再灌注损伤（MIRI）大鼠急性心肌缺血（MI）及“内关”（PC 6）区Toll样受体4（TLR 4）、髓样分化因子88（MyD 88）和核因子κB（NF-κB）mRNA表达的影响，以探讨其改善MIRI的机制。
48只雄性Wistar大鼠随机分为对照组、对照＋电针组、假手术组、模型组、电针组和假电针组（每组8只）。采用结扎左冠状动脉前降支30 min后再灌注的方法建立MIRI模型。建模前，分别对PC 6或假PC 6进行电针预处理30 min，每天1次，共5天。记录建模前后及再灌注0.25 h后标准肢体导联Ⅱ的心电图。采用实时荧光定量PCR检测PC 6组织中TLR 4、MyD 88和NF-κB基因的表达水平。
与对照组比较，模型组心电图J点抬高明显（<0.01），提示急性心肌梗死，电针组J点抬高明显低于模型组和假电针组（<0.01）。与对照组比较，模型组PC 6区TLR 4、MyD 88和NF-κB mRNA表达水平明显上调（<0.01）。与模型组比较，电针预处理组TLR 4、MyD 88和NF-κB mRNA表达水平升高明显受到抑制（<0.05）。对照组、对照＋电针组和假手术组之间以及模型组和假电针组之间TLR 4、MyD 88和NF-κB mRNA表达水平差异均无统计学意义（>0.05）。
电针预处理可改善心肌缺血，降低MIRI大鼠PC 6区TLR 4、MyD 88和NF-κB mRNA表达，提示局部皮肤TLR 4/MyD 88/NF-κB信号通路抑制参与电针刺激信号输入的起始-传递-放大过程，从而减轻MIRI。
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