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  • Title: [Electroacupuncture promotes angiogenesis in MIRI rats by modulating the AMPK/KLF2 signaling pathway].
    Author: Liu QQ, Zhang HR, Gu YH.
    Journal: Zhen Ci Yan Jiu; ; 49(9):902-908. PubMed ID: 39401826.
    Abstract:
    OBJECTIVES: To observe the effect of electroacupuncture(EA) on adenosine 5'-monophosphate-activated protein kinase (AMPK)/Kruppel-like factor 2 (KLF2) signaling pathway in ischemic myocardial tissues of rats, so as to explore the underlying mechanism of EA in attenuating myocardial ischemia-reperfusion injury (MIRI) through mediating angiogenesis. METHODS: Male SD rats were randomly divided into sham operation group, model group and EA group, with 10 rats in each group. The MIRI model was established by ligation of the anterior descending branch of the left coronary artery. Twenty-four hours after modeling, the rats in the EA group were given EA (2 Hz/100 Hz, 2 mA) at "Neiguan" (PC6) for 20 min each time, once a day for 5 consecutive days. Echocardiography was used to detect cardiac ejection fraction (EF) to evaluate cardiac function. HE staining was used to observe the morphological changes in rat myocardial tissue. Immunohistochemistry was used to detect the density of neovascularization in rat ischemic myocardium. Western blot and ELISA were used to detect the phosphorylated(p)-AMPK, AMPK, KLF2, vascular endothelial growth factor (VEGF) protein expression levels, and VEGF receptor 2 (VEGFR2) content in rat ischemic myocardial tissue, respectively. RESULTS: After modeling, compared with the sham operation group, rats in the model group had decreased EF(P<0.01), significant myocardial fiber damage with inflammatory cell infiltration, increased neovascular density (P<0.05), increased p-AMPK, AMPK, VEGF protein expression levels and VEGFR2 content in myocardial ischemic tissues(P<0.05, P<0.01), and decreased protein expression level of KLF2 (P<0.05). After EA intervention, compared with the model group, rats in the EA group had elevated EF(P<0.01), significantly reduced myocardial fiber damage, reduced inflammatory cell infiltration, increased neovascular density(P<0.01), and elevated p-AMPK, AMPK, KLF2, and VEGF protein expression levels and VEGFR2 content in the myocardial ischemic tissue (P<0.01). CONCLUSIONS: EA may promote angiogenesis, attenuate myocardial injury, and achieve cardioprotective effects in MIRI rats by regulating the expression of AMPK/KLF2 signaling pathway in myocardial tissues. 目的: 探讨电针通过调控腺苷酸活化蛋白激酶（AMPK）/Kruppel样因子2（KLF2）信号通路介导血管新生减轻心肌缺血再灌注损伤（MIRI）的效应机制。方法: SD大鼠随机分为假手术组、模型组和电针组，每组10只。采用左冠状动脉前降支结扎法制备MIRI模型。电针组电针“内关”，每次20 min，每天1次，连续5 d。采用超声心动图检测大鼠心脏射血分数（EF）评价心功能；HE染色观察大鼠心肌组织形态学变化；免疫组织化学法检测大鼠缺血心肌新生血管密度（MVD）；Western blot法检测大鼠缺血心肌组织磷酸化AMPK（p-AMPK）、AMPK、KLF2、血管内皮生长因子（VEGF）蛋白表达量；ELISA法检测大鼠缺血心肌组织血管内皮生长因子受体2（VEGFR2）含量。结果: 与假手术组比较，模型组大鼠EF降低（P<0.01），心肌纤维明显损伤并伴炎性细胞浸润，MVD增加（P<0.05），心肌缺血组织p-AMPK、AMPK、VEGF蛋白表达及VEGFR2含量升高（P<0.05，P<0.01），KLF2表达降低（P<0.05）。与模型组比较，电针组大鼠EF升高（P<0.01），心肌纤维损伤明显减轻、炎性细胞浸润减少，MVD增加（P<0.01），心肌缺血组织p-AMPK、AMPK、KLF2、VEGF蛋白表达及VEGFR2含量升高（P<0.01）。结论: 电针可能通过调控AMPK/KLF2信号通路的表达来促进MIRI大鼠血管新生，减轻心肌损伤，达到心肌保护效应。.
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