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针刺预处理对大鼠缺血心肌线粒体通透孔开放的调节
引用本文:宋春华,丁续,王保叶,付嘉明,徐红飞,公维志,董勤建,李晓艳,郭丹丹,金艳红,闫珺,亢连茹.针刺预处理对大鼠缺血心肌线粒体通透孔开放的调节[J].长春中医药大学学报,2018(3):422-425.
作者姓名:宋春华  丁续  王保叶  付嘉明  徐红飞  公维志  董勤建  李晓艳  郭丹丹  金艳红  闫珺  亢连茹
作者单位:黑龙江中医药大学,哈尔滨,150040 仪陇县人民医院,四川南充,637600
基金项目:黑龙江省自然科学基金面上项目"针灸治疗疑难病及对神经-内分泌-免疫网络系统的调节研究"(H2015035)
摘    要:目的研究电针心俞预处理对大鼠缺血心肌线粒体通透孔开放的调节。方法将大鼠随机分为空白组、模型组、针刺心俞预处理组(实验组)及缺血预处理组(对照组),采用活体大鼠心左冠脉前降支结扎法复制MIRI模型。空白组:造模前固定30 min不针刺,1次/d,连续15 d。模型组:造模前同空白组,MIRI造模。实验组:造膜前15 d开始针刺,1次/d,30 min/次,共15 d。对照组:造模前同空白组,造模行冠脉结扎前先阻断血流5 min,再灌流5 min,连续3次,共30 min缺血预处理。心肌缺血造模成功后即刻、24、48 h检测心肌细胞m PTP开放程度及对Bal-2、Caspase-3表达的影响。结果模型组激光共聚焦显微镜(LSCM)观察心肌线粒体绿色荧光对比空白组明显减弱,表明其m PTP活性显著减低(P0.01)。与模型组比,对照组与实验组即刻组LSCM观察示,心肌线粒体荧光强度明显减低,但对照组与实验组即刻组各项指标差异无统计学意义(P0.05)。实验24、48 h组与对照组及实验组即刻组对照LSCM观察线粒体荧光强度有增强(P0.05或P0.01)。实验组与对照组均可减轻MIRI损伤;且可能实验组24 h组为最佳治疗方案。实验组可下调Caspase-3、上调Bal-2。结论电针心俞预处理对缺血后不同时间心肌的保护作用存在差异,并且治疗作用随时间的改变呈增强-峰值-减弱趋势。电针心俞预处理对心肌MIRI有保护作用,其机制可能是通过调节MIRI过程中心肌m PTP的开放,减少线粒体凋亡,减轻心肌损伤有关。

关 键 词:针灸推拿学  针刺预处理  缺血预处理  激光共聚焦显微镜  线粒体通透性转换孔  acupuncture  and  massage  acupuncture  preconditioning  ischemic  preconditioning  the  laser  confocal  microscope  mitochondrial  permeability  transition  pore

Effect of acupuncture pretreatment on opening of mitochondrial permeability in rats with ischemic myocardium
SONG Chunhua,DING Xu,WANG Baoye,FU Jiaming,XU Hongfei,GONG Weizhi,DONG Qinjian,LI Xiaoyan,GUO Dandan,JIN Yanhong,YAN Jun,KANG Lianru.Effect of acupuncture pretreatment on opening of mitochondrial permeability in rats with ischemic myocardium[J].Journal of Changchun College of Traditional Chinese Medicine,2018(3):422-425.
Authors:SONG Chunhua  DING Xu  WANG Baoye  FU Jiaming  XU Hongfei  GONG Weizhi  DONG Qinjian  LI Xiaoyan  GUO Dandan  JIN Yanhong  YAN Jun  KANG Lianru
Abstract:Objective To investigate molecular mechanism by study of Xinshu electrical acupuncture preconditioning on the opening of mitochondrial permeability in rats with ischemic myocardium.Methods Rats were randomly divided into blank group, model group, acupuncture Xinshu preconditioning group (experimental group) and ischemic preconditioning group (control group). MIRI model was established by ligation of left anterior descending coronary artery in living rat heart. Blank group: fixed 30 min without acupuncture once a day, continuous 15 days.Model group: same blank group before modeling and control group.In the experimental group, acupuncturewas started at 15 d before making the film, 1 times /d, and 30min/ times, with a total of 15 d. In the control group, the blood flow was blocked for 5 minutes before coronary artery ligation and reperfusion for 5 minutes, followed by 30 min ischemic preconditioning for 3 consecutive times.Immediately after the successful establishment of myocardial ischemia model, 24, 48 hours.The open degree of mPTP and its effect on the expression of Bal-2 Caspase-3 in cardiomyocytes were detected.Results Model group dyed myocardial mitochondria green fluorescent compared with the blank group was reduced obviously, the experiment result shows that the mitochondrial membrane permeability transition pore activity of model group was significantly reduced (P<0.01). Compared with the model group, LSCM observation showed that the myocardial mitochondrial fluorescence intensity was significantly decreased in the control group and the experimental group, but there was no significant difference between the control group and the immediate experimental group (P>0.05). Test 24 h, 48 h group mitochondria fluorescence intensity have a certain enhancement (P<0.05 orP<0.01) observed compared with control group and test 0h group. Experiment data shows that test and control group both can reduce MIRI.Test group can down-regulate Caspase-3 and up-regulate Bal-2.Conclusion The protective effect of electroacupuncture pretreatment on Xinshu at different time after myocardial ischemia and the difference of therapeutic effect was enhanced with the change of the time to peak - weakening trend. Electroacupuncture Xinshu pretreatment has protective effects on myocardial Miri, its mechanism may be through the regulation of MIRI during myocardial MPTP open, reduce mitochondrial apoptosis, reduce myocardial injury.
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