摘要
目的:观察内关电针预处理对心肌缺血再灌注损伤(MIRI)大鼠心肌细胞蛋白激酶(PKC)、ATP敏感性钾通道(KATP)、线粒体膜通透性转换孔(MPTP)的影响。探讨针刺内关穴防治心血管疾病及经穴脏腑理论相关机制。方法:将40只SD雄性大鼠随机分为假手术组、缺血再灌注组、电针内关组和电针环跳组,每组10只。电针内关组和电针环跳组在造模前,分别给予电针刺激20min/d。共7d。采用左冠状动脉前降支上、中1/3交界处结扎法造模,所有动物造模后予以心电图监测,结扎40min,再灌注60min,取心肌组织。观察PKC、内向整流钾通道(Kir6.1)、MPTP三个指标的变化及心肌细胞超微结构的改变。结果:缺血再灌注组PKC、Kir6.1较假手术组明显降低(P〈0.01),MPTP较假手术组明显升高(P〈0.01);电针内关组PKC、Kir6.1较缺血再灌注组及电针环跳组明显升高(P〈0.01),MPTP较缺血再灌注组及电针环跳组明显降低(P〈0.01);缺血再灌注组与电针环跳组组间比较差异无统计学意义(P〉0.05)。结论:电针预处理内关穴通过激活PKC,增加KATP开放,抑制MPTP开放来对抗心肌缺血再灌注损伤,从而对心肌产生保护作用。
Objective:To observe the effect of nei guan(PC 6) electroacupuncture(EA) preconditioning on point zang-fu theory. Method:There were 40 male SD rats randomly divided into sham operation group, MIRI group,EA nei guan group and EA huan tiao group,10 rats in each group. Before establishing the MIRI animal model,EA nei guan group and EA huan tiao group were given EA 20 minutes per day,for 7 days. Ligation was conducted in the upper and middle 1/3 artery to establish the animal model. After establishing the junction of the left anterior descending coronary animal model,electrocardiography was conducted. (P〈0.01),compared with the sham operation group. In EA nei guart group,PKC and Kir6.1 significantly increased(P〈0.01) ,while MPTP significantly decreased(P〈0.01),compared with MIRI group and EA huan tiao group. There was no significant guan EA preconditioning through difference between MIRI group and EA group(P〉0.05). Conclusion:Nei activation of PKC ,increases the opening of KATP,and inhibits the opening of MPTP,to relieve MIRI,and therefore it has a protective effect on the myocardium.
出处
《山东中医杂志》
2018年第3期237-240,共4页
Shandong Journal of Traditional Chinese Medicine
基金
国家自然科学基金项目(编号:81574080)
湖南省中医药管理局课题(编号:2015211)
湖南省高校创新平台开放基金项目(编号:15k093)
2015年针灸推拿学湖南省“十二五”重点学科开放基金资助项目(序号:06)
关键词
心肌缺血再灌注损伤
电针
内关
心肌细胞蛋白激酶
ATP敏感性钾通道
线粒体膜通透性转换孔
myocardial ischemia reperfusion injury
electroacupuncture
nei guan (PC 6)
protein kinaseC
ATP sensitive potassium channels
mitochondrialpermeability transition pore