NDLI: Interval training suppresses nod-like receptor protein 3 inflammasome activation to improve cardiac function in myocardial infarction rats by hindering the activation of the transforming growth factor-β1 pathway

Content Provider	Springer Nature : BioMed Central
Author	Wei, Wei Xie, Ping Wang, Xuemei
Abstract	Objective Myocardial infarction (MI) -induced cardiac dysfunction can be attenuated by aerobic exercises. This study explored the mechanism of interval training (IT) regulating cardiac function in MI rats, providing some theoretical basis for clarifying MI pathogenesis and new ideas for clinically treating MI. Methods Rats were subjected to MI modeling, IT intervention, and treatments of the Transforming growth factor-β1 (TGF-β1) pathway or the nod-like receptor protein 3 (NLRP3) activators. Cardiac function and hemodynamic indicator alterations were observed. Myocardial pathological damage and fibrosis, reactive oxygen species (ROS) level, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, MDA content, inflammasome-associated protein levels, and inflammatory factor levels were assessed. The binding between TGF-β1 and receptor was detected. Results MI rats exhibited decreased left ventricle ejection fraction (LVEF), left ventricle fractional shortening (LVFS), left ventricular systolic pressure (LVSP), positive and negative derivates max/min (dP/dt max/min) and increased left ventricular end-systolic pressure (LVEDP), a large number of scar areas in myocardium, disordered cell arrangement and extensive fibrotic lesions, increased TGF-β1 and receptor binding, elevated ROS level and MDA content and weakened SOD, CAT and GSH-Px activities, and up-regulated NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and cleaved-caspase-1 levels, while IT intervention caused ameliorated cardiac function. IT inactivated the TGF-β1 pathway to decrease oxidative stress in myocardial tissues of MI rats and inhibit NLRP3 inflammasome activation. Activating NLRP3 partially reversed IT-mediated improvement on cardiac function in MI rats. Conclusion IT diminished oxidative stress in myocardial tissues and suppressed NLRP3 inflammasome activation via inactivating the TGF-β1 pathway, thus improving the cardiac function of MI rats.
Related Links	https://cardiothoracicsurgery.biomedcentral.com/counter/pdf/10.1186/s13019-024-02756-1.pdf
Ending Page	12
Page Count	12
Starting Page	1
File Format	HTM / HTML
ISSN	17498090
DOI	10.1186/s13019-024-02756-1
Journal	Journal of Cardiothoracic Surgery
Issue Number	1
Volume Number	19
Language	English
Publisher	BioMed Central
Publisher Date	2024-05-10
Access Restriction	Open
Subject Keyword	Cardiac Surgery Thoracic Surgery Myocardial infarction Interval training TGF-β1 NLRP3 Oxidative stress Cardiac function
Content Type	Text
Resource Type	Article
Subject	Surgery Cardiology and Cardiovascular Medicine Pulmonary and Respiratory Medicine
Journal Impact Factor	1.5/2023
5-Year Journal Impact Factor	1.6/2023

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