Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury

Aim: Hyperleptinemia potentiates the effects of many atherogenic factors, such as inflammation, platelet aggregation, migration, hypertrophy, proliferation of vascular smooth muscle cells, and endothelial cell dysfunction. The present study analysed the effects of long-term hyperleptinemia in an in...

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Autores principales: Ekaterina A. Polyakova, Evgeny N. Mikhaylov, Michael M. Galagudza, Evgeny V. Shlyakhto
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Lenguaje:EN
Publicado: Elsevier 2021
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spelling oai:doaj.org-article:ec77f7a4774e4dbdbec59fe4395a89102021-12-02T05:03:26ZHyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury2405-844010.1016/j.heliyon.2021.e08491https://doaj.org/article/ec77f7a4774e4dbdbec59fe4395a89102021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2405844021025949https://doaj.org/toc/2405-8440Aim: Hyperleptinemia potentiates the effects of many atherogenic factors, such as inflammation, platelet aggregation, migration, hypertrophy, proliferation of vascular smooth muscle cells, and endothelial cell dysfunction. The present study analysed the effects of long-term hyperleptinemia in an in vivo myocardial ischemia-reperfusion model to demonstrate whether the in vivo deleterious effect also affects cardiac structure and function. Main methods: Rats were subcutaneously administered leptin for 8 days to estimate the involvement of the JAK/STAT pathway. Data from 58 male Wistar rats were included in the final analysis. Myocardial infarction (MI) was modelled by the 30-minute ligation of the main left coronary artery followed by 120-minute reperfusion. Hemodynamic measurements, electrocardiography monitoring, echocardiography, myocardial infarct size and area at risk, blood biochemical parameters, leptin, IL-6, TNF-alpha, FGF-21, and cardiomyocyte morphology were measured. The expression of JAK2, p-JAK2, STAT3, p-STAT3 was assessed by Western Blot analysis. Statistical analyses were performed using IBM SPSS Statistics v.26. Key findings: Eight-day hyperleptinemia in rats leads to an increase in blood pressure and heart rate, myocardial hypertrophy, impaired LV function, the frequency of ischemic arrhythmias, dyslipidemia, systemic inflammation, and the size of induced myocardial infarction. Significance: The blockade of the JAK/STAT signalling pathway effectively reverses the negative effects of leptin, including increased blood pressure and total cholesterol.Ekaterina A. PolyakovaEvgeny N. MikhaylovMichael M. GalagudzaEvgeny V. ShlyakhtoElsevierarticleLeptinJAK/STAT pathwayMyocardial infarctionHemodynamicsArrhythmiasDyslipidemiaScience (General)Q1-390Social sciences (General)H1-99ENHeliyon, Vol 7, Iss 11, Pp e08491- (2021)
institution DOAJ
collection DOAJ
language EN
topic Leptin
JAK/STAT pathway
Myocardial infarction
Hemodynamics
Arrhythmias
Dyslipidemia
Science (General)
Q1-390
Social sciences (General)
H1-99
spellingShingle Leptin
JAK/STAT pathway
Myocardial infarction
Hemodynamics
Arrhythmias
Dyslipidemia
Science (General)
Q1-390
Social sciences (General)
H1-99
Ekaterina A. Polyakova
Evgeny N. Mikhaylov
Michael M. Galagudza
Evgeny V. Shlyakhto
Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
description Aim: Hyperleptinemia potentiates the effects of many atherogenic factors, such as inflammation, platelet aggregation, migration, hypertrophy, proliferation of vascular smooth muscle cells, and endothelial cell dysfunction. The present study analysed the effects of long-term hyperleptinemia in an in vivo myocardial ischemia-reperfusion model to demonstrate whether the in vivo deleterious effect also affects cardiac structure and function. Main methods: Rats were subcutaneously administered leptin for 8 days to estimate the involvement of the JAK/STAT pathway. Data from 58 male Wistar rats were included in the final analysis. Myocardial infarction (MI) was modelled by the 30-minute ligation of the main left coronary artery followed by 120-minute reperfusion. Hemodynamic measurements, electrocardiography monitoring, echocardiography, myocardial infarct size and area at risk, blood biochemical parameters, leptin, IL-6, TNF-alpha, FGF-21, and cardiomyocyte morphology were measured. The expression of JAK2, p-JAK2, STAT3, p-STAT3 was assessed by Western Blot analysis. Statistical analyses were performed using IBM SPSS Statistics v.26. Key findings: Eight-day hyperleptinemia in rats leads to an increase in blood pressure and heart rate, myocardial hypertrophy, impaired LV function, the frequency of ischemic arrhythmias, dyslipidemia, systemic inflammation, and the size of induced myocardial infarction. Significance: The blockade of the JAK/STAT signalling pathway effectively reverses the negative effects of leptin, including increased blood pressure and total cholesterol.
format article
author Ekaterina A. Polyakova
Evgeny N. Mikhaylov
Michael M. Galagudza
Evgeny V. Shlyakhto
author_facet Ekaterina A. Polyakova
Evgeny N. Mikhaylov
Michael M. Galagudza
Evgeny V. Shlyakhto
author_sort Ekaterina A. Polyakova
title Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
title_short Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
title_full Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
title_fullStr Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
title_full_unstemmed Hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
title_sort hyperleptinemia results in systemic inflammation and the exacerbation of ischemia-reperfusion myocardial injury
publisher Elsevier
publishDate 2021
url https://doaj.org/article/ec77f7a4774e4dbdbec59fe4395a8910
work_keys_str_mv AT ekaterinaapolyakova hyperleptinemiaresultsinsystemicinflammationandtheexacerbationofischemiareperfusionmyocardialinjury
AT evgenynmikhaylov hyperleptinemiaresultsinsystemicinflammationandtheexacerbationofischemiareperfusionmyocardialinjury
AT michaelmgalagudza hyperleptinemiaresultsinsystemicinflammationandtheexacerbationofischemiareperfusionmyocardialinjury
AT evgenyvshlyakhto hyperleptinemiaresultsinsystemicinflammationandtheexacerbationofischemiareperfusionmyocardialinjury
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