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。
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（P0.01）,and obviously increased in the EA-PC 6group（P0.01）,but not in the EA-non-acupoint group（P0.05）.The expression levels of myocardial CLC-2and CLCA proteins were significantly up-regulated in the model group compared with the control group（P0.01）and markedly down-regulated in the EA-PC 6group（not in the EAnon-acupoint group）in comparison with the model group（P0.01）,suggesting a specificity of effects of EA-PC 6in improving myocardial injury and down-regulating CLC-2and CLCA protein expression.Concl
作者
成泽东
陈以国
李晓梅
覃佩兰
梁繁荣
荣培晶
CHENG Ze-dong CHEN Yi-guo LI Xiao-mei QIN Pei-lan LIANG Fan-rong RONG Pei-jing(College of Acumoxibustion and Massage, Liaoning University of Traditional Chinese Medicine, Shen yang 110847, China 1.College of Acu-moxibustion and Massage, Chengdu University of Traditional Chinese Medicine, Chengdu 61007 2. China Academy of Chinese Medical Sciences ,Beijing 10070)
出处
《针刺研究》
CAS
CSCD
北大核心
2016年第5期423-428,共6页
Acupuncture Research
基金
国家重点基础研究发展计划("973"计划)资助项目(No.2012CB 518503)
关键词
急性心肌缺血
电针
内关
CLC-2氯离子通道
钙激活的氯离子通道
Acute myocardial ischemia
Electroacupuncture
Neiguan（PC 6）
Chloride channel（CLC）-2
Calcium（Ca2＋）-activated chloride channel accessory（CLCA）
