Ling Yun Gu, Cheng Gao Jia, Zuo Zhen Sheng, Wen Long Jiang, Zhuo Wen Xu, Wei Zhang Li, Jun You Cui, Hua Zhang
{"title":"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","authors":"Ling Yun Gu, Cheng Gao Jia, Zuo Zhen Sheng, Wen Long Jiang, Zhuo Wen Xu, Wei Zhang Li, Jun You Cui, Hua Zhang","doi":"10.14740/cr1705","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusions: </strong>FGF21 may exert cardioprotective effects by inhibiting I/R injury-induced NETs via AMPK.</p>","PeriodicalId":9424,"journal":{"name":"Cardiology Research","volume":"15 5","pages":"404-414"},"PeriodicalIF":1.4000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11483118/pdf/","citationCount":"0","resultStr":"{\"title\":\"Fibroblast Growth Factor 21 Suppressed Neutrophil Extracellular Traps Induced by Myocardial Ischemia/Reperfusion Injury via Adenosine Monophosphate-Activated Protein Kinase.\",\"authors\":\"Ling Yun Gu, Cheng Gao Jia, Zuo Zhen Sheng, Wen Long Jiang, Zhuo Wen Xu, Wei Zhang Li, Jun You Cui, Hua Zhang\",\"doi\":\"10.14740/cr1705\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusions: </strong>FGF21 may exert cardioprotective effects by inhibiting I/R injury-induced NETs via AMPK.</p>\",\"PeriodicalId\":9424,\"journal\":{\"name\":\"Cardiology Research\",\"volume\":\"15 5\",\"pages\":\"404-414\"},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11483118/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cardiology Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14740/cr1705\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/11 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiology Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14740/cr1705","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/11 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Fibroblast Growth Factor 21 Suppressed Neutrophil Extracellular Traps Induced by Myocardial Ischemia/Reperfusion Injury via Adenosine Monophosphate-Activated Protein Kinase.
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.
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.
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