Wang Junmeng, Yuan Jing, Cai Yun, Fu Shuping, Li Minhui, Hong Hao, Lu Shengfeng, Zhu Bingmei
Ministry of Education Key Laboratory of Acupuncture and Medicine, Nanjing University of CM, Nanjing 210023, Jiangsu Province, China.
Zhongguo Zhen Jiu. 2018 May 12;38(5):5133-8. doi: 10.13703/j.0255-2930.2018.05.017.
To observe the effects of electroacupuncture (EA) on inflammatory reaction of acute myocardial ischemia (MI) in mice, and to explore its action mechanism.
Forty adult male C57BL/6 mice were randomly divided into a control group, a sham operation group, a model group and an EA group, 10 mice in each one. The model was established in the model group and EA group by ligating the left anterior descending branch of coronary artery. The mice in the EA group were treated with EA at "Neiguan" (PC 6) with 2 mA of intensity and 2 Hz /100 Hz of frequency; EA was given 30 min per treatment, once a day for totally 5 days. The mice in the control group and model group were treated with immobilization and no EA was given. The mice in the sham operation group were not treated with ligating at the left anterior descending branch of coronary artery, but the remaining procedure was identical to the model group. The electrocardiogram was recorded and △ST was calculated to evaluate the model. TTC and HE staining methods were applied to evaluate the infarct size and pathologic change of myocardial tissue, respectively. Western blot method was applied to test the protein expression levels of tumor necrosis factor-α (TNF-α), nuclear factor-κB p65 (NF-κB p65), interleukin-1β (IL-1β) and interleukin-8 (IL-8).
Compared with the sham operation group, the S-T segments in the model group and EA group were increased obviously after modeling (both <0.01), indicating the MI model was established successfully. The TTC and HE staining results indicated, compared with the sham operation group, the model group had larger infarction size (<0.01), more myocardial fibers injury and inflammatory infiltration; compared with the model group, the infarction size of the EA group was significantly reduced (<0.01), and the myocardial fibers injury and inflammatory infiltration were improved. Compared with the control group, the protein expression levels in the sham operation group were similar (all >0.05); compared with the sham operation group, the expression levels of TNF-α, NF-κB p65, IL-1β and IL-8 were significantly increased in the model group (<0.01, <0.05); compared with the model group, the expression levels of TNF-α, NF-κB p65, IL-1β and IL-8 were significantly reduced in the EA group (all <0.05).
EA might reduce the protein expression levels of TNF-α, NF-κB p65, IL-1β and IL-8 in cardiac muscle tissue to inhibit inflammatory reaction and achieve myocardial protective effect in mice with acute myocardial ischemia.
观察电针（EA）对小鼠急性心肌缺血（MI）炎症反应的影响，并探讨其作用机制。
40只成年雄性C57BL/6小鼠随机分为对照组、假手术组、模型组和电针组，每组10只。模型组和电针组通过结扎冠状动脉左前降支建立模型。电针组小鼠取“内关”（PC 6）穴，以2 mA强度、2 Hz/100 Hz频率进行电针治疗；每次治疗30分钟，每天1次，共5天。对照组和模型组小鼠进行固定，不给予电针治疗。假手术组小鼠不结扎冠状动脉左前降支，但其余操作与模型组相同。记录心电图并计算△ST以评估模型。分别采用TTC和HE染色法评估心肌梗死面积和心肌组织病理变化。采用蛋白质免疫印迹法检测肿瘤坏死因子-α（TNF-α）、核因子-κB p65（NF-κB p65）、白细胞介素-1β（IL-1β）和白细胞介素-8（IL-8）的蛋白表达水平。
与假手术组相比，模型组和电针组建模后S-T段明显抬高（均P<0.01），表明MI模型成功建立。TTC和HE染色结果显示，与假手术组相比，模型组梗死面积更大（P<0.01），心肌纤维损伤及炎症浸润更多；与模型组相比，电针组梗死面积明显减小（P<0.01），心肌纤维损伤及炎症浸润得到改善。与对照组相比，假手术组蛋白表达水平相近（均P>0.05）；与假手术组相比，模型组TNF-α、NF-κB p65、IL-1β和IL-8表达水平明显升高（P<0.01，P<0.05）；与模型组相比，电针组TNF-α、NF-κB p65、IL-1β和IL-8表达水平明显降低（均P<0.05）。
电针可能通过降低心肌组织中TNF-α、NF-κB p65、IL-1β和IL-8的蛋白表达水平来抑制炎症反应，从而对急性心肌缺血小鼠发挥心肌保护作用。
