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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/再灌注损伤诱导的中性粒细胞胞外陷阱

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

作者信息

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

机构信息

Department of Cardiology, Jiangyin Hospital Affiliated to Nantong University, Jiangyin, China.

The Jiangyin Clinical College of Xuzhou Medical University, Jiangyin, China.

出版信息

Cardiol Res. 2024 Oct;15(5):404-414. doi: 10.14740/cr1705. Epub 2024 Oct 11.

DOI:10.14740/cr1705
PMID:39420979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11483118/
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.

摘要

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诱捕网（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

诱导建立小鼠心肌I/R损伤模型，用免疫荧光法对心肌组织进行染色以评估NETs。使用PicoGreen试剂盒定量血清NETs水平。此外，通过Wes全自动蛋白质印迹定量分析系统评估单磷酸腺苷（AMP）激活的蛋白激酶（AMPK）和FGF21的表达水平。而且，使用AMPK抑制剂和激动剂预处理H9c2细胞建立缺氧/复氧（H/R）模型，以进一步探究FGF21与AMPK之间的关系。

结果

与对照组相比，I/R小鼠血清NETs水平显著更高，心肌组织中形成了大量NETs（97.63±11.45对69.65±3.33，P<0.05）。然而，FGF21预处理小鼠的NETs水平有所逆转（P<0.05）。进一步研究表明，FGF21增强了AMPK表达，在抑制AMPK后显著增加，在促进AMPK后降低（P<0.05）。

结论

FGF21可能通过AMPK抑制I/R损伤诱导的NETs发挥心脏保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6593/11483118/1fac4cf4eef1/cr-15-404-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6593/11483118/763f2252a934/cr-15-404-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6593/11483118/1fac4cf4eef1/cr-15-404-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6593/11483118/78a54da1bb16/cr-15-404-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6593/11483118/1fac4cf4eef1/cr-15-404-g008.jpg

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Elevated serum FGF21 levels predict heart failure during hospitalization of STEMI patients after emergency percutaneous coronary intervention.血清 FGF21 水平升高可预测 STEMI 患者急诊经皮冠状动脉介入治疗后住院期间心力衰竭的发生。
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