Cardioprotection of mAb2G4/ODN/lip on Myocardial Ischemia-Reperfusion Injury via Inhibiting the NF-κB Signaling Pathway

IF 3.4 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Zujin Xu, Zhuoran Wei, Yali Zhu, Guoqing Jing, Liufang Chen, Jia Zhan, Yun Wu
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引用次数: 0

Abstract

Substantial evidence suggests that the interventions of NF-κB would likely effectively prevent inflammatory response and reduce myocardial damage in the ischemic myocardium. And the NF-кB decoy ODN is a specific inhibitor that suppresses the expression of NF-κB. Herein, we revealed the effect and possible mechanism of mAb2G4/ODN/lip on myocardial ischemia-reperfusion injury (MI/RI). As shown in the results, post-treatment with mAb2G4/ODN/lip improved the impaired histological morphology in the MI/RI model and elevated cell viability in the H/R model. The mAb2G4/ODN/lip complex inhibited the NLRP3 signaling pathway and decreased the expression of LDH, IL-1β, TNF-α, IL-6, and MDA. Mechanistically, we demonstrated that post-treatment with mAb2G4/ODN/lip exerted protective effects against I/R injuries by inhibiting the NF-кB-related inflammatory response. In summary, the present study may offer a novel therapeutic strategy for treating MI/RI.

Abstract Image

mAb2G4/ODN/lip通过抑制NF-κB信号通路对心肌缺血再灌注损伤的心脏保护作用
大量证据表明,NF-κB干预可能有效预防缺血心肌的炎症反应,减轻心肌损伤。NF-кB诱饵ODN是抑制NF-κB表达的特异性抑制剂。本研究揭示了mAb2G4/ODN/lip在心肌缺血再灌注损伤(MI/RI)中的作用及其可能机制。结果显示,mAb2G4/ODN/lip处理后改善了MI/RI模型中受损的组织学形态,提高了H/R模型中的细胞活力。mAb2G4/ODN/lip复合物抑制NLRP3信号通路,降低LDH、IL-1β、TNF-α、IL-6和MDA的表达。在机制上,我们证明mAb2G4/ODN/lip治疗后通过抑制NF-кB-related炎症反应对I/R损伤具有保护作用。综上所述,本研究可能为治疗MI/RI提供一种新的治疗策略。
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来源期刊
Cardiovascular Therapeutics
Cardiovascular Therapeutics 医学-心血管系统
CiteScore
5.60
自引率
0.00%
发文量
55
审稿时长
6 months
期刊介绍: Cardiovascular Therapeutics (formerly Cardiovascular Drug Reviews) is a peer-reviewed, Open Access journal that publishes original research and review articles focusing on cardiovascular and clinical pharmacology, as well as clinical trials of new cardiovascular therapies. Articles on translational research, pharmacogenomics and personalized medicine, device, gene and cell therapies, and pharmacoepidemiology are also encouraged. Subject areas include (but are by no means limited to): Acute coronary syndrome Arrhythmias Atherosclerosis Basic cardiac electrophysiology Cardiac catheterization Cardiac remodeling Coagulation and thrombosis Diabetic cardiovascular disease Heart failure (systolic HF, HFrEF, diastolic HF, HFpEF) Hyperlipidemia Hypertension Ischemic heart disease Vascular biology Ventricular assist devices Molecular cardio-biology Myocardial regeneration Lipoprotein metabolism Radial artery access Percutaneous coronary intervention Transcatheter aortic and mitral valve replacement.
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