Effects of Electroacupuncture on Expression of Myocardial Chloride Channel-2 and CLCA Proteins in Mice with Acute Myocardial Ischemia

CHENG Ze-dong; CHEN Yi-guo; LI Xiao-mei; QIN Pei-lan; LIANG Fan-rong; RONG Pei-jing

doi:10.13702/j.1000-0607.2016.05.011

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Effects of Electroacupuncture on Expression of Myocardial Chloride Channel-2 and CLCA Proteins in Mice with Acute Myocardial Ischemia

更新时间：2023-08-11

- Effects of Electroacupuncture on Expression of Myocardial Chloride Channel-2 and CLCA Proteins in Mice with Acute Myocardial Ischemia
- Acupuncture Research Vol. 41, Issue 5, Pages: 423-428(2016)
- 作者机构：
  
  1. 辽宁中医药大学针灸推拿学院
  2. 成都中医药大学针灸推拿学院
  3. 中国中医科学院针灸研究所
- 作者简介：
- 基金信息：
- DOI：10.13702/j.1000-0607.2016.05.011
  CLC：
- Published：2016
- 稿件说明：
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CHENG Ze-dong, CHEN Yi-guo, LI Xiao-mei, et al. Effects of Electroacupuncture on Expression of Myocardial Chloride Channel-2 and CLCA Proteins in Mice with Acute Myocardial Ischemia[J]. Acupuncture research, 2016, 41(5): 423-428.
DOI：

CHENG Ze-dong, CHEN Yi-guo, LI Xiao-mei, et al. Effects of Electroacupuncture on Expression of Myocardial Chloride Channel-2 and CLCA Proteins in Mice with Acute Myocardial Ischemia[J]. Acupuncture research, 2016, 41(5): 423-428. DOI： 10.13702/j.1000-0607.2016.05.011.

摘要

目的:观察电针"内关"穴对急性心肌缺血小鼠心肌CLC-2氯离子通道[chloride channel-2

CLC-2]、钙激活的氯离子通道(calcium-activated chloride channel accessory

CLCA)蛋白表达的影响

探讨针刺抗心肌缺血的可能作用机制。方法:30只基因敲除ASIC 3-/-小鼠随机分为空白组、模型组、内关组、列缺组、非经非穴组。采用多点皮下注射异丙肾上腺素制备急性心肌缺血模型。内关组电针双侧"内关"穴

列缺组电针双侧"列缺"穴

非经非穴组电针"天枢"穴与"神阙"穴连线中点

每天治疗1次

共治疗7d。造模前后记录Ⅱ导联心电图ST段电压幅值

HE染色观察小鼠心肌组织病理变化

比色法检测血清超氧化物歧化酶(SOD)活性

Western blot法检测心肌组织CLC-2、CLCA蛋白表达。结果:造模后各组小鼠Ⅱ导联心电图ST段明显抬高

与造模前比较差异具有统计学意义(P<0.05)。HE染色结果显示

模型组、列缺组、非经非穴组与空白组比较有不同程度的心肌细胞缺血区;与模型组比较

内关组有明显改善。与空白组比较

模型组小鼠血清SOD活性明显下降(P<0.01);与模型组比较

内关组可明显抑制SOD的下降(P<0.01)。与空白组比较

模型组CLC-2、CLCA蛋白表达水平显著升高(P<0.01);与模型组比较

内关组CLC-2、CLCA蛋白表达显著降低(P<0.01)。结论:针刺"内关"穴可显著降低急性心肌缺血小鼠心肌组织CLC-2、CLCA蛋白表达水平

可能是针刺治疗小鼠急性心肌缺血的作用机制之一。

Abstract

Objective To observe the influence of electroacupuncture stimulation(EA)of"Neiguan"(PC 6)/"Lieque"(LU 7)on ST segment of electrocardiogram(ECG)and the expression of myocardiac chloride channel(CLC)-2and calcium(Ca2+)-activated chloride channel accessory(CLCA)proteins in acute myocardial ischemia(AMI)mice

so as to explore its mechanisms underlying improvement of AMI.Methods Thirty ASIC 3-/-knock out mice were randomly divided into control

AMI model

EA-Neiguan(PC 6)

EA-Lieque(LU 7)and EA-non-acupoint groups.The AMI model was induced by multiple subcutaneous injection of isoprenaline(ISO

0.5g/L

20mg/kg).EA was applied to bilateral PC 6

LU 7

or non-acupoint[the midpoint between"Tianshu"(ST 25)and "Shenque"(CV 8)]for 20 min

once daily for 7days.The ST segment of ECG of the standardⅡlimb-lead was recorded using a PowerLab data acquisition device

the change of myocardial histology observed by using microscope after HE staining

the activity of serum superoxide dismutase(SOD)detected using Colorimetric method

and the expression of CLC-2and CLCA proteins of the left ventricle myocardium detected by Western blot.Results Outcomes of HE staining showed that the ischemic injury(sarcoplasm swelling and necrosis

etc.)of the left ventrical myocardial tissue after modeling was relatively milder in the EA-PC 6group

not in the EA-non-acupoint group.The SOD activity was significantly lower in the model group than in the control group(P<0.01)

and obviously increased in the EA-PC 6group(P<0.01)

but not in the EA-non-acupoint group(P>0.05).The expression levels of myocardial CLC-2and CLCA proteins were significantly up-regulated in the model group compared with the control group(P<0.01)and markedly down-regulated in the EA-PC 6group(not in the EAnon-acupoint group)in comparison with the model group(P<0.01)

suggesting a specificity of effects of EA-PC 6in improving myocardial injury and down-regulating CLC-2and CLCA protein expression.Conclusion EA of"Neiguan"(PC 6)can effectively suppress the increase of expression of CLC-2and CLCA proteins in the left ventricle myocardium

which may contribute to its effect in relieving myocardial injury in mice.

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