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Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways

OBJECTIVE: To investigate whether exercise preconditioning (EP) improves the rat cardiac dysfunction induced by exhaustive exercise (EE) through regulating NOD-like receptor protein 3 (NLRP3) inflammatory pathways and to confirm which intensity of EP is better. METHOD: Ninety healthy male Sprague Da...

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Autores principales: Li, Yuemin, Xu, Peng, Wang, Yang, Zhang, Junshi, Yang, Mei, Chang, Yumei, Zheng, Ping, Huang, Heling, Cao, Xuebin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301185/
https://www.ncbi.nlm.nih.gov/pubmed/32595731
http://dx.doi.org/10.1155/2020/5809298
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author Li, Yuemin
Xu, Peng
Wang, Yang
Zhang, Junshi
Yang, Mei
Chang, Yumei
Zheng, Ping
Huang, Heling
Cao, Xuebin
author_facet Li, Yuemin
Xu, Peng
Wang, Yang
Zhang, Junshi
Yang, Mei
Chang, Yumei
Zheng, Ping
Huang, Heling
Cao, Xuebin
author_sort Li, Yuemin
collection PubMed
description OBJECTIVE: To investigate whether exercise preconditioning (EP) improves the rat cardiac dysfunction induced by exhaustive exercise (EE) through regulating NOD-like receptor protein 3 (NLRP3) inflammatory pathways and to confirm which intensity of EP is better. METHOD: Ninety healthy male Sprague Dawley rats were randomly divided into five groups: a control group (CON), exhaustive exercise group (EE), low-, middle-, and high-intensity exercise precondition and exhaustive exercise group (LEP + EE, MEP + EE, HEP + EE group). We established the experimental model by referring to Bedford's motion load standard to complete the experiment. Then, the pathological changes of the myocardium were observed under a light microscope. Biomarker of myocardial injury in serum and oxidative stress factor in myocardial tissue were evaluated by ELISAs. The cardiac function parameters were detected using a Millar pressure and volume catheter. The levels of thioredoxin-interacting protein (TXNIP), thioredoxin protein (TRX), nuclear transcription factor kappa B(p65) (NF-ĸB(p65)), NLRP3, and cysteinaspartate specific proteinase 1 (Caspase-1) protein in rats' myocardium were detected by western blotting. RESULTS: 1. The myocardial structures of three EP + EE groups were all improved compared with EE groups. 2. The levels of the creatine phosphating-enzyme MB (CK-MB), reactive oxygen species (ROS), interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor alpha (TNF-α) in three EP + EE groups were all increased compared with CON but decreased compared with the EE group (P < 0.05). 3. Compared with the CON group, slope of end-systolic pressure volume relationship (ESPVR), ejection fraction (EF), and peak rate of the increase in pressure (dP/dt(max)) all dropped to the lowest level in the EE group (P < 0.05), while the values of cardiac output (CO), stroke volume (SV), end-systolic volume (Ves), end-diastolic volume (Ved), and relaxation time constant (Tau) increased in the EE group (P < 0.05). 4. Compared with the CON group, the expression levels of TXNIP, NF-ĸB(p65), NLRP3, and Caspase-1 all increased obviously in the other groups (P < 0.05); meanwhile, they were all decreased in three EP + EE groups compared with the EE group (P < 0.05). 5. NLRP3 was positively correlated with heart rate, IL-6, and ROS, but negatively correlated with EF (P < 0.01). CONCLUSION: EP protects the heart from EE-induced injury through downregulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 inflammatory signaling pathways. Moderate intensity EP has the best protective effect.
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spelling pubmed-73011852020-06-25 Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways Li, Yuemin Xu, Peng Wang, Yang Zhang, Junshi Yang, Mei Chang, Yumei Zheng, Ping Huang, Heling Cao, Xuebin Evid Based Complement Alternat Med Research Article OBJECTIVE: To investigate whether exercise preconditioning (EP) improves the rat cardiac dysfunction induced by exhaustive exercise (EE) through regulating NOD-like receptor protein 3 (NLRP3) inflammatory pathways and to confirm which intensity of EP is better. METHOD: Ninety healthy male Sprague Dawley rats were randomly divided into five groups: a control group (CON), exhaustive exercise group (EE), low-, middle-, and high-intensity exercise precondition and exhaustive exercise group (LEP + EE, MEP + EE, HEP + EE group). We established the experimental model by referring to Bedford's motion load standard to complete the experiment. Then, the pathological changes of the myocardium were observed under a light microscope. Biomarker of myocardial injury in serum and oxidative stress factor in myocardial tissue were evaluated by ELISAs. The cardiac function parameters were detected using a Millar pressure and volume catheter. The levels of thioredoxin-interacting protein (TXNIP), thioredoxin protein (TRX), nuclear transcription factor kappa B(p65) (NF-ĸB(p65)), NLRP3, and cysteinaspartate specific proteinase 1 (Caspase-1) protein in rats' myocardium were detected by western blotting. RESULTS: 1. The myocardial structures of three EP + EE groups were all improved compared with EE groups. 2. The levels of the creatine phosphating-enzyme MB (CK-MB), reactive oxygen species (ROS), interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor alpha (TNF-α) in three EP + EE groups were all increased compared with CON but decreased compared with the EE group (P < 0.05). 3. Compared with the CON group, slope of end-systolic pressure volume relationship (ESPVR), ejection fraction (EF), and peak rate of the increase in pressure (dP/dt(max)) all dropped to the lowest level in the EE group (P < 0.05), while the values of cardiac output (CO), stroke volume (SV), end-systolic volume (Ves), end-diastolic volume (Ved), and relaxation time constant (Tau) increased in the EE group (P < 0.05). 4. Compared with the CON group, the expression levels of TXNIP, NF-ĸB(p65), NLRP3, and Caspase-1 all increased obviously in the other groups (P < 0.05); meanwhile, they were all decreased in three EP + EE groups compared with the EE group (P < 0.05). 5. NLRP3 was positively correlated with heart rate, IL-6, and ROS, but negatively correlated with EF (P < 0.01). CONCLUSION: EP protects the heart from EE-induced injury through downregulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 inflammatory signaling pathways. Moderate intensity EP has the best protective effect. Hindawi 2020-06-08 /pmc/articles/PMC7301185/ /pubmed/32595731 http://dx.doi.org/10.1155/2020/5809298 Text en Copyright © 2020 Yuemin Li et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Li, Yuemin
Xu, Peng
Wang, Yang
Zhang, Junshi
Yang, Mei
Chang, Yumei
Zheng, Ping
Huang, Heling
Cao, Xuebin
Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways
title Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways
title_full Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways
title_fullStr Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways
title_full_unstemmed Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways
title_short Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸB(p65)/NLRP3 Inflammatory Pathways
title_sort different intensity exercise preconditions affect cardiac function of exhausted rats through regulating txnip/trx/nf-ĸb(p65)/nlrp3 inflammatory pathways
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301185/
https://www.ncbi.nlm.nih.gov/pubmed/32595731
http://dx.doi.org/10.1155/2020/5809298
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