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.