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首页|期刊导航|江苏大学学报(医学版)|FKBP5通过影响细胞代谢参与缺氧缺糖/复氧复糖诱导的大鼠H9C2心肌细胞损伤

FKBP5通过影响细胞代谢参与缺氧缺糖/复氧复糖诱导的大鼠H9C2心肌细胞损伤

鲍思旭 吴奇勇

江苏大学学报(医学版)2025,Vol.35Issue(3):230-237,8.
江苏大学学报(医学版)2025,Vol.35Issue(3):230-237,8.DOI:10.13312/j.issn.1671-7783.y240158

FKBP5通过影响细胞代谢参与缺氧缺糖/复氧复糖诱导的大鼠H9C2心肌细胞损伤

FKBP5 participates in oxygen-glucose deprivation/reperfusion-induced rat H9C2 cardiomyocytes injury by regulating cellular metabolism

鲍思旭 1吴奇勇1

作者信息

  • 1. 常州市第二人民医院胸心外科,江苏 常州 213002||南京医科大学第三附属医院胸心外科,江苏 常州 213002
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摘要

Abstract

Objective:To explore the mechanism of FK506 binding protein 5(FKBP5,also known as the FKBP51)in rat H9C2 cardiomyocytes injury induced by oxygen-glucose deprivation/reperfusion(OGD/R).Methods:H9C2 cells were divided into the blank control group,OGD/R group and OGD/R+small interfering RNA silencing FKBP5(OGD/R+si-FKBP5)group.The contents of lactate dehydrogenase(LDH),creatine kinase isozyme(CK-MB)and cardiac troponin I(cTnI)in each group of H9C2 cells were detected by enzyme-linked immunosorbent assay(ELISA),and metabolites differences and signaling pathways were analyzed by principal component analysis(PCA)and enrichment analysis.Results:ELISA results showed that silencing FKBP5 significantly suppressed the increased levels of LDH,CK-MB,and cTnI(P<0.05 and P<0.001).Metabolomics analysis revealed 49 differential metabolites induced by OGD/R treatment,while silencing of FKBP5 resulted in 53 differential metabolites.Pathway hierarchy analysis indicated that OGD/R-induced differential metabolites were involved in amino acid metabolism,endocrine system,membrane transport,and signal transduction pathways,while these pathways showed significant adaptive changes after silencing FKBP5.KEGG pathway analysis further demonstrated that these differential metabolites were enriched in key signaling pathways such as mTOR,FoxO,and cGMP-PKG.The metabolites of these signaling pathway also showed significant adaptive changes after silencing FKBP5.Conclusion:The results suggest that silencing FKBP5 may alleviate OGD/R-induced myocardial injury by regulating multiple key metabolites and signaling pathways.

关键词

心肌缺血再灌注损伤/FK506结合蛋白5/代谢组学/信号通路/细胞代谢

Key words

myocardial ischemia-reperfusion injury/FK506 binding protein 5/metabolomics/signaling pathways/cellular metabolism

分类

临床医学

引用本文复制引用

鲍思旭,吴奇勇..FKBP5通过影响细胞代谢参与缺氧缺糖/复氧复糖诱导的大鼠H9C2心肌细胞损伤[J].江苏大学学报(医学版),2025,35(3):230-237,8.

基金项目

常州市科技局重大科技项目(CE20205047) (CE20205047)

江苏大学学报(医学版)

1671-7783

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