电针心经对急性心肌缺血大鼠海马CA1区氧化应激及BDNF信号通路相关蛋白表达的影响  

Effect of Electroacupuncture at the Heart Meridian on Oxidative Stress and Expression of Proteins Related to the Brain-derived Neurotrophic Factor Signaling Pathway in the Hippocampal CA1 Region of Acute Myocardial Ischemia Rats

作　　者：童思佳 王堃 左海燕 王磊 吴生兵[2] 周美启[3,4] TONG Sijia;WANG Kun;ZUO Haiyan;WANG Lei;WU Shengbing;ZHOU Meiqi(Graduate School of Anhui University of Chinese Medicine,Anhui Hefei 230012,China;Key Laboratory of Xin an Medicine,Ministry of Education,Anhui Hefei 230038,China;Institute of Acupuncture and Meridian,Anhui University of Chinese Medicine,Anhui Hefei 230012,China;Bozhou Institute of Chinese Medicine,Anhui Academy of Chinese Medicine,Anhui Bozhou 236800,China)

机构地区：[1]安徽中医药大学研究生院,安徽合肥230012 [2]新安医学教育部重点实验室,安徽合肥230038 [3]安徽中医药大学针灸经络研究所,安徽合肥230012 [4]安徽省中医药科学院亳州中医药研究所,安徽亳州236800

出　　处：《安徽中医药大学学报》2023年第2期26-31,共6页Journal of Anhui University of Chinese Medicine

基　　金：国家自然科学基金项目(82004462);安徽省中医药领军人才建设项目;浙江中医药大学科研开放基金项目(ZYXYB2019002)。

摘　　要：目的观察电针心经“神门-通里”段对急性心肌缺血(acute myocardial ischemia,AMI)大鼠海马CA1区超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)、脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、酪氨酸蛋白激酶B(tyrosine protein kinase,TrkB)、蛋白激酶B(protein kinase B,Akt)、磷酸化Akt(phosphorylated Akt,p-Akt)等变化的影响,分析电针心经改善AMI引发海马神经细胞损伤的机制。方法将大鼠按照随机数字表法分为伪手术组、模型组、电针组,每组10只。采用冠状动脉左前降支结扎法制备AMI大鼠模型,伪手术组仅穿线不结扎。电针组予以双侧“神门-通里”段电针治疗,电流强度1 mA,频率2 Hz,每次30 min,连续3 d,其余两组不予治疗。用PowerLab 16导生理记录仪采集心电图,并分析ST段电位;苏木精-伊红染色法观察大鼠心肌组织形态;采用ELISA法检测大鼠海马CA1区SOD、MDA含量;尼氏染色法观察大鼠海马CA1区病理形态变化;TUNEL染色法观察大鼠海马CA1区细胞凋亡率;Western blot法检测大鼠海马CA1区BDNF、TrkB、Akt、p-Akt蛋白表达水平。结果与伪手术组比较,模型组大鼠心电图ST段明显抬高(P<0.05);心肌纤维肿胀断裂,间隙扩大;海马CA1区MDA水平增加(P<0.05)、SOD水平减少(P<0.05);神经细胞数量减少,凋亡率增加(P<0.05);BDNF、TrkB蛋白表达水平及p-Akt/Akt均显著降低(P<0.05)。与模型组比较,电针组大鼠心电图ST段明显降低(P<0.05);心肌纤维部分扭曲,排列较整齐,病理改变减轻;海马CA1区MDA含量减少(P<0.05),SOD含量增加(P<0.05);神经细胞数量增加,凋亡率降低(P<0.05);BDNF、TrkB蛋白表达水平及p-Akt/Akt比值均显著升高(P<0.05)。大鼠海马CA1区BDNF、TrkB及p-Akt/Akt水平与ST段电位存在显著负相关关系。结论电针心经能有效改善AMI导致的海马神经细胞损伤,其作用可能与改善氧化应激,激活BDNF信号通路相关蛋白表达有关。Objective To investigate the effect of electroacupuncture(EA)at the“Shenmen-Tongli”segment of the heart meridian on superoxide dismutase(SOD),malondialdehyde(MDA),brain-derived neurotrophic factor(BDNF),tyrosine kinase receptor B(TrkB),protein kinase B(Akt),and phosphorylated Akt(p-Akt)in the hippocampal CA1 region of acute myocardial ischemia(AMI)rats,as well as the mechanism of EA at the heart meridian in improving hippocampal neuronal injury due to AMI.Methods A total of 30 rats were divided into sham-operation group,model group,and EA group using a random number table,with 10 rats in each group.Ligation of the left anterior descending coronary artery was performed to establish a rat model of AMI,and the rats in the sham-operation group were given suture without ligation.The rats in the EA group were given EA at the“Shenmen-Tongli”segment,with a current intensity of 1 mA and a frequency of 2 Hz,for 30 minutes each time for 3 consecutive days,and those in the other two groups were not given any treatment.The PowerLab 16-lead physiograph was used to obtain the electrocardiogram and analyze ST-segment potential;HE staining was used to observe the pathology of myocardial tissue;ELISA was used to measure the content of SOD and MDA in the hippocampal CA1 region;Nissl staining was used to observe the pathomorphological changes of the hippocampal CA1 region;TUNEL staining was used to observe cell apoptosis rate in the hippocampal CA1 region;Western blot was used to measure the protein expression levels of BDNF,TrkB,Akt,and p-Akt in the hippocampal CA1 region.Results Compared with the sham-operation group,the model group had the following changes:marked ST-segment elevation(P<0.05);swelling and rupture of myocardial fibers with widened spaces;a significant increase in the content of MDA(P<0.05)and a significant reduction in the content of SOD(P<0.05)in the hippocampal CA1 region;a significant reduction in the number of neurons and a significant increase in apoptosis rate(P<0.05);significant reductions in the pr

关 键 词：急性心肌缺血 电针 海马 氧化应激 脑源性神经营养因子 

分 类 号：R542.22[医药卫生—心血管疾病]