| Purpose:To systematically organize and analyze the effector mechanism ofmyocardial ischemia rats’ cardiac function and the chloride channel relatedgene expression in myocardium, study the targeting regulatory effect of chloridechannel’s response by needling the acupoints of corresponding meridians as wellas sort out its biological basis and features on chloride channel in myocardiumthrough observing the index change of cardiac ultrasound and the chloridechannel related gene, the index change is obtained by needling LU7ã€HT7ã€PC6and non-acupoints of the research objectï¼myocardial ischemia rats models.Material and Methods:15rats were randomly selected from the75healthymale SD rats (SPF) as the blank control group, bred conventionally. Rest of therats were divided into4groups randomly. The model groupã€Neiguan point groupã€Lieque point groupã€non-acupoint group, each group had15rats, and were raisedin separated rooms with usual diet. Rat models of myocardial ischemia in thesefour groups were established by multi-point injecting isoproterenol (ISO). InNeiguan point groupã€Lieque point group and non-acupoints group respectivelyacupunctured both sides of Neiguan pointã€Lieque pointã€non-acupoints withelectroacupuncture therapy for20minutes daily and lasted for a week. Testedcardiac functions of rats with color doppler ultrasonic imaging, and appliedreal-time quantitative PCR to detect the expression level of voltage-dependentchloride channel’s transmembrane conductance regulatory factor CLC-2ã€CLC-3gene in rat myocardium.Result:1. Compared with blank control group, rat hearts in model groupã€Lieque groupand non-acupoint group obviously are enlarged and heart activities amplitudesclearly decrease leading to the decline of left ventricular ejection fraction as well as weakness of rats cardiac function evidently, it has statisticalsignificance (p<0.01); compared with model group, the left ventricular ejectionfraction of rats in the Neiguan group obviously increase, left ventricularend-diastolic diameter and end-systolic diameter improve clearly, havingstatistical significance (p<0.01); difference of the left ventricular ejectionfractionã€left ventricular end-diastolic diameter and end-systolic diameter ofrats in model groupã€Lieque group and non-acupoint group has no statisticalsignificance (p>0.05).2. Compared with blank control group, the expression level of chloride channelCLC-2ã€CLC-3gene in rat myocardium increases clearly in model groupã€Liequegroup and non-acupoint group, having statistical significance (p<0,01);compared with model group, the expression level of chloride channel CLC-2ã€CLC-3gene in rat myocardium obviously decreases in Neiguan group, havingstatistical significance (p<0.01).Conclusion:1. Acupuncturing PC6can improve the cardiac function of acute myocardialischemia rats.It proves that needling PC6can treat the weakness of rats’ cardiac function;compared with LU7and non-acupoints, PC6presents the significant specificeffect of treatment along meridians.2. Acupuncturing PC6can regulate the content of voltage-dependent chloridechannel CLC-2and CLC-3gene expression.Needling PC6regulates the voltage-dependent chloride channel in ratmyocardium through regulating the content of voltage-dependent chloride channelCLC-2and CLC-3gene expression, which may be one of the mechanism for myocardialinjury caused by myocardial ischemia, and PC6has more effect on targeting ofrat’s myocardium than LU7and non-acupoints.3. Acupuncturing acupoints has specific effectPC6has specific effect on protection of myocardial ischemia, which may be achieved through regulating the expression level of the voltage-dependentchloride channel’s CLC-2ã€CLC-3gene in rat myocardium. |