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OBJECTIVE

This study aims to investigate the activation of the PPARγ/NF-κB pathway and its influence on macrophage M2 polarization induced by acupuncture at the Neiguan acupoint. Additionally, it seeks to explore the potential mechanisms by which electroacupuncture treatment may facilitate the reduction of inflammation in rats subjected to myocardial ischemia-reperfusion injury (MIRI).

METHODS

SD rats were randomly assigned to four groups: sham operation, model, electroacupuncture, and inhibitor, with 12 rats in each group. The left anterior descending branch of the coronary artery was ligated to establish the MIRI rat model. Electroacupuncture intervention at the bilateral Neiguan acupoints commenced 24 h post-chest closure, lasting for 30 min once daily over three consecutive days. Myocardial infarction was assessed through electrocardiography, while cardiac function was evaluated via echocardiography 24 h after modeling. The morphology and structure of myocardial tissues were examined using HE staining. Myocardial tissue levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) were measured by ELISA in each group of rats. The expression of the M1 macrophage marker inducible nitric oxide synthase (iNOS) and the M2 macrophage marker arginase-1 (Arg-1) in myocardial tissues was analyzed using immunohistochemistry (IHC). Detection of macrophage polarization status in myocardial tissue by flow cytometry. Additionally, peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear transcription factor-κB (NF-κB) expression in myocardial tissues was assessed using Western blotting (WB).

RESULTS

Compared with the sham-operated group, rats in the model group exhibited a significant decrease in ejection fraction (EF) ( < 0.01), along with notable myocardial fiber damage characterized by inflammatory cell infiltration. Additionally, there was an elevated expression of IL-6, TGF-β, iNOS, CD-86 and phosphorylated p65 (p-p65) in myocardial tissue ( < 0.01, < 0.01, < 0.05, < 0.05 and < 0.01, respectively). In contrast, rats in the electroacupuncture group demonstrated an increase in EF ( < 0.01) compared to the model group. Myocardial fiber damage was significantly ameliorated, inflammatory cell infiltration was reduced. Furthermore, the expression of IL-10, TGF-β, Arg-1, CD-163 and PPARγ in cardiac muscle tissue was increased ( < 0.01, < 0.01, < 0.05, < 0.05 and < 0.01, respectively). Conversely, when compared to the electroacupuncture group, the EF of rats in the inhibitor group was significantly reduced ( < 0.05), with pronounced myocardial fiber damage and accompanying inflammatory cell infiltration. Additionally, IL-6, TGF-β, iNOS CD-86 and p-p65 expression in myocardial tissue was increased ( < 0.01, < 0.01, < 0.05, < 0.05 and < 0.01, respectively).

CONCLUSION

Electroacupuncture may ameliorate myocardial MIRI by activating the PPARγ/NF-κB pathway, promoting polarization of macrophages towards the M2 type, and reducing inflammatory damage in myocardial tissues.

OBJECTIVE

METHODS

RESULTS

CONCLUSION

目的

本研究旨在探讨针刺内关穴对PPARγ/NF-κB通路的激活作用及其对巨噬细胞M2极化的影响。此外，还试图探索电针治疗促进心肌缺血再灌注损伤（MIRI）大鼠炎症减轻的潜在机制。

方法

将SD大鼠随机分为四组：假手术组、模型组、电针组和抑制剂组，每组12只。结扎冠状动脉左前降支建立MIRI大鼠模型。胸部闭合24小时后开始双侧内关穴电针干预，每天一次，持续30分钟，连续三天。通过心电图评估心肌梗死情况，建模24小时后通过超声心动图评估心功能。用HE染色检查心肌组织的形态和结构。用ELISA法检测每组大鼠心肌组织中白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、白细胞介素-10（IL-10）和转化生长因子-β（TGF-β）的水平。用免疫组织化学（IHC）分析心肌组织中M1巨噬细胞标志物诱导型一氧化氮合酶（iNOS）和M2巨噬细胞标志物精氨酸酶-1（Arg-1）的表达。通过流式细胞术检测心肌组织中巨噬细胞的极化状态。此外，用蛋白质印迹法（WB）评估心肌组织中过氧化物酶体增殖物激活受体γ（PPARγ）和核转录因子-κB（NF-κB）的表达。

结果

与假手术组相比，模型组大鼠射血分数（EF）显著降低（<0.01），伴有明显的心肌纤维损伤，表现为炎症细胞浸润。此外，心肌组织中IL-6、TGF-β、iNOS、CD-86和磷酸化p65（p-p65）的表达升高（分别为<0.01、<0.01、<0.05、<0.05和<0.01）。相比之下，电针组大鼠的EF较模型组增加（<0.01）。心肌纤维损伤明显改善，炎症细胞浸润减少。此外，心肌组织中IL-10、TGF-β、Arg-1、CD-163和PPARγ的表达增加（分别为<0.01、<0.01、<0.05、<0.05和<0.01）。相反，与电针组相比，抑制剂组大鼠的EF显著降低（<0.05），心肌纤维损伤明显，伴有炎症细胞浸润。此外，心肌组织中IL-6、TGF-β、iNOS、CD-86和p-p65的表达增加（分别为<0.01、<0.01、<0.05、<0.05和<0.01）。