Fibroblast Growth Factor 21 Suppressed Neutrophil Extracellular Traps Induced by Myocardial Ischemia/Reperfusion Injury via Adenosine Monophosphate-Activated Protein Kinase.

IF 1.4 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS

Cardiology Research Pub Date : 2024-10-01 Epub Date: 2024-10-11 DOI:10.14740/cr1705

Ling Yun Gu, Cheng Gao Jia, Zuo Zhen Sheng, Wen Long Jiang, Zhuo Wen Xu, Wei Zhang Li, Jun You Cui, Hua Zhang

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Abstract

Background: Previous investigations have established the anti-inflammatory properties of fibroblast growth factor 21 (FGF21). However, the specific mechanism through which FGF21 mitigates myocardial ischemia/reperfusion (I/R) injury by inhibiting neutrophil extracellular traps (NETs) remains unclear.

Methods: A mice model of myocardial I/R injury was induced, and myocardial tissue was stained with immunofluorescence to assess NETs. Serum NETs levels were quantified using a PicoGreen kit. In addition, the expression levels of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and FGF21 were evaluated by Wes fully automated protein blotting quantitative analysis system. Moreover, a hypoxia/reoxygenation (H/R) model was established using AMPK inhibitor and agonist pretreated H9c2 cells to further explore the relationship between FGF21 and AMPK.

Results: Compared with the control group, serum NETs levels were significantly higher in I/R mice, and a large number of NETs were formed in myocardial tissues (97.63 ± 11.45 vs. 69.65 ± 3.33, P < 0.05). However, NETs levels were reversed in FGF21 pretreated mice (P < 0.05). Further studies showed that FGF21 enhanced AMPK expression, which was significantly increased after inhibition of AMPK and decreased after promotion of AMPK (P < 0.05).

Conclusions: FGF21 may exert cardioprotective effects by inhibiting I/R injury-induced NETs via AMPK.

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成纤维细胞生长因子 21 通过单磷酸腺苷激活的蛋白激酶抑制心肌缺血/再灌注损伤诱发的中性粒细胞胞外陷阱

背景：先前的研究已证实成纤维细胞生长因子 21（FGF21）具有抗炎特性。然而，FGF21通过抑制中性粒细胞胞外捕获物（NETs）减轻心肌缺血再灌注（I/R）损伤的具体机制仍不清楚：方法：诱导小鼠心肌I/R损伤模型，用免疫荧光染色心肌组织以评估NETs。使用 PicoGreen 试剂盒对血清 NETs 水平进行量化。此外，单磷酸腺苷（AMP）活化蛋白激酶（AMPK）和 FGF21 的表达水平也通过 Wes 全自动蛋白印迹定量分析系统进行了评估。此外，还利用AMPK抑制剂和激动剂预处理的H9c2细胞建立了缺氧/再氧合（H/R）模型，以进一步探讨FGF21与AMPK之间的关系：结果：与对照组相比，I/R小鼠血清NETs水平明显升高，心肌组织中形成了大量NETs（97.63 ± 11.45 vs. 69.65 ± 3.33，P < 0.05）。然而，FGF21 预处理小鼠的 NETs 水平得到逆转（P < 0.05）。进一步的研究表明，FGF21能增强AMPK的表达，抑制AMPK后，NETs表达显著增加，而促进AMPK后，NETs表达减少（P＜0.05）：结论：FGF21可通过AMPK抑制I/R损伤诱导的NET，从而发挥心脏保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cardiology Research CARDIAC & CARDIOVASCULAR SYSTEMS-

CiteScore

2.50

自引率

0.00%

发文量

期刊介绍： Cardiology Research is an open access, peer-reviewed, international journal. All submissions relating to basic research and clinical practice of cardiology and cardiovascular medicine are in this journal''s scope. This journal focuses on publishing original research and observations in all cardiovascular medicine aspects. Manuscript types include original article, review, case report, short communication, book review, letter to the editor.