Cardio and neuroprotective consequences of swimming training in ovariectomized rats
- Autores
- Ibañez, Alejandro Martín; Godoy Coto, Joshua; Martínez, Valeria Romina; Yeves, Alejandra del Milagro; Dolcetti, Franco Juan Cruz; Cervellini, Sofía; Echavarría, Lucía; Vélez Rueda, Jorge Omar; Lofeudo, Juan Manuel; Portiansky, Enrique Leo; Bellini, María José; Aiello, Ernesto Alejandro; Ennis, Irene Lucía; De Giusti, Verónica Celeste
- Año de publicación
- 2024
- Idioma
- español castellano
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Cardiovascular (CV) disease is the major cause of mortality. Estrogens (E) exert multiple CV and neuroprotective effects. During menopause CV and cognitive pathologies increase dramatically. At present, it is known that E exert many of their beneficial effects through the G protein-coupled estrogen receptor (GPER). Exercise reduces the risk of developing CV diseases. Sodium/proton exchanger (NHE-1) is overexpressed in ovariectomized (OVX) rats, probably due by the increase in reactive oxidative species (ROS). Insulin-like growth factor 1 (IGF-1), the main humoral mediator of exercise, inhibits the NHE-1. We aim to explore the subcellular mechanisms involved in the heart and brain impact of physiological exercise in OVX rats. We speculate that physical training, via IGF-1, prevents the increase in ROS; improving heart and brain physiological functions during menopause. Exercise diminished cardiac ROS production and increased catalase (CAT) activity in OVX rats. In concordance, IGF-1 treatment reduces brain ROS, surely contributing to the improvement in brain behavior. Moreover, aerobic routine was able to prevent, and IGF-1 therapy to revert, NHE-1 hyperactivity in OVX rats. Finally, our results confirm the proposed signaling pathway as: IGF-1/PI3K-AKT/NO. Surprisingly, GPER inhibitor (G36) was able to abolish IGF-1 effect, suggesting that directly or indirectly GPER is part of IGF-1 pathway. We propose that IGF-1 is the main responsible for the protective effect of aerobic training both in heart and brain in OVX rats. Moreover, we showed that not only it is possible to prevent, but also to revert the menopause-induced NHE-1 hyperactivity by exercise/IGF-1 cascade.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares - Materia
-
Ciencias Médicas
ovariectomized rats
IGF-1
cardioprotection
neuroprotection
exercise training - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
.jpg)
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/182281
Ver los metadatos del registro completo
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Cardio and neuroprotective consequences of swimming training in ovariectomized ratsIbañez, Alejandro MartínGodoy Coto, JoshuaMartínez, Valeria RominaYeves, Alejandra del MilagroDolcetti, Franco Juan CruzCervellini, SofíaEchavarría, LucíaVélez Rueda, Jorge OmarLofeudo, Juan ManuelPortiansky, Enrique LeoBellini, María JoséAiello, Ernesto AlejandroEnnis, Irene LucíaDe Giusti, Verónica CelesteCiencias Médicasovariectomized ratsIGF-1cardioprotectionneuroprotectionexercise trainingCardiovascular (CV) disease is the major cause of mortality. Estrogens (E) exert multiple CV and neuroprotective effects. During menopause CV and cognitive pathologies increase dramatically. At present, it is known that E exert many of their beneficial effects through the G protein-coupled estrogen receptor (GPER). Exercise reduces the risk of developing CV diseases. Sodium/proton exchanger (NHE-1) is overexpressed in ovariectomized (OVX) rats, probably due by the increase in reactive oxidative species (ROS). Insulin-like growth factor 1 (IGF-1), the main humoral mediator of exercise, inhibits the NHE-1. We aim to explore the subcellular mechanisms involved in the heart and brain impact of physiological exercise in OVX rats. We speculate that physical training, via IGF-1, prevents the increase in ROS; improving heart and brain physiological functions during menopause. Exercise diminished cardiac ROS production and increased catalase (CAT) activity in OVX rats. In concordance, IGF-1 treatment reduces brain ROS, surely contributing to the improvement in brain behavior. Moreover, aerobic routine was able to prevent, and IGF-1 therapy to revert, NHE-1 hyperactivity in OVX rats. Finally, our results confirm the proposed signaling pathway as: IGF-1/PI3K-AKT/NO. Surprisingly, GPER inhibitor (G36) was able to abolish IGF-1 effect, suggesting that directly or indirectly GPER is part of IGF-1 pathway. We propose that IGF-1 is the main responsible for the protective effect of aerobic training both in heart and brain in OVX rats. Moreover, we showed that not only it is possible to prevent, but also to revert the menopause-induced NHE-1 hyperactivity by exercise/IGF-1 cascade.Facultad de Ciencias MédicasCentro de Investigaciones Cardiovasculares2024-11-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf2317-2334http://sedici.unlp.edu.ar/handle/10915/182281spainfo:eu-repo/semantics/altIdentifier/issn/2509-2723info:eu-repo/semantics/altIdentifier/doi/10.1007/s11357-024-01422-7info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:49:43Zoai:sedici.unlp.edu.ar:10915/182281Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:49:43.948SEDICI (UNLP) - Universidad Nacional de La Platafalse |
| dc.title.none.fl_str_mv |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| title |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| spellingShingle |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats Ibañez, Alejandro Martín Ciencias Médicas ovariectomized rats IGF-1 cardioprotection neuroprotection exercise training |
| title_short |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| title_full |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| title_fullStr |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| title_full_unstemmed |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| title_sort |
Cardio and neuroprotective consequences of swimming training in ovariectomized rats |
| dc.creator.none.fl_str_mv |
Ibañez, Alejandro Martín Godoy Coto, Joshua Martínez, Valeria Romina Yeves, Alejandra del Milagro Dolcetti, Franco Juan Cruz Cervellini, Sofía Echavarría, Lucía Vélez Rueda, Jorge Omar Lofeudo, Juan Manuel Portiansky, Enrique Leo Bellini, María José Aiello, Ernesto Alejandro Ennis, Irene Lucía De Giusti, Verónica Celeste |
| author |
Ibañez, Alejandro Martín |
| author_facet |
Ibañez, Alejandro Martín Godoy Coto, Joshua Martínez, Valeria Romina Yeves, Alejandra del Milagro Dolcetti, Franco Juan Cruz Cervellini, Sofía Echavarría, Lucía Vélez Rueda, Jorge Omar Lofeudo, Juan Manuel Portiansky, Enrique Leo Bellini, María José Aiello, Ernesto Alejandro Ennis, Irene Lucía De Giusti, Verónica Celeste |
| author_role |
author |
| author2 |
Godoy Coto, Joshua Martínez, Valeria Romina Yeves, Alejandra del Milagro Dolcetti, Franco Juan Cruz Cervellini, Sofía Echavarría, Lucía Vélez Rueda, Jorge Omar Lofeudo, Juan Manuel Portiansky, Enrique Leo Bellini, María José Aiello, Ernesto Alejandro Ennis, Irene Lucía De Giusti, Verónica Celeste |
| author2_role |
author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Ciencias Médicas ovariectomized rats IGF-1 cardioprotection neuroprotection exercise training |
| topic |
Ciencias Médicas ovariectomized rats IGF-1 cardioprotection neuroprotection exercise training |
| dc.description.none.fl_txt_mv |
Cardiovascular (CV) disease is the major cause of mortality. Estrogens (E) exert multiple CV and neuroprotective effects. During menopause CV and cognitive pathologies increase dramatically. At present, it is known that E exert many of their beneficial effects through the G protein-coupled estrogen receptor (GPER). Exercise reduces the risk of developing CV diseases. Sodium/proton exchanger (NHE-1) is overexpressed in ovariectomized (OVX) rats, probably due by the increase in reactive oxidative species (ROS). Insulin-like growth factor 1 (IGF-1), the main humoral mediator of exercise, inhibits the NHE-1. We aim to explore the subcellular mechanisms involved in the heart and brain impact of physiological exercise in OVX rats. We speculate that physical training, via IGF-1, prevents the increase in ROS; improving heart and brain physiological functions during menopause. Exercise diminished cardiac ROS production and increased catalase (CAT) activity in OVX rats. In concordance, IGF-1 treatment reduces brain ROS, surely contributing to the improvement in brain behavior. Moreover, aerobic routine was able to prevent, and IGF-1 therapy to revert, NHE-1 hyperactivity in OVX rats. Finally, our results confirm the proposed signaling pathway as: IGF-1/PI3K-AKT/NO. Surprisingly, GPER inhibitor (G36) was able to abolish IGF-1 effect, suggesting that directly or indirectly GPER is part of IGF-1 pathway. We propose that IGF-1 is the main responsible for the protective effect of aerobic training both in heart and brain in OVX rats. Moreover, we showed that not only it is possible to prevent, but also to revert the menopause-induced NHE-1 hyperactivity by exercise/IGF-1 cascade. Facultad de Ciencias Médicas Centro de Investigaciones Cardiovasculares |
| description |
Cardiovascular (CV) disease is the major cause of mortality. Estrogens (E) exert multiple CV and neuroprotective effects. During menopause CV and cognitive pathologies increase dramatically. At present, it is known that E exert many of their beneficial effects through the G protein-coupled estrogen receptor (GPER). Exercise reduces the risk of developing CV diseases. Sodium/proton exchanger (NHE-1) is overexpressed in ovariectomized (OVX) rats, probably due by the increase in reactive oxidative species (ROS). Insulin-like growth factor 1 (IGF-1), the main humoral mediator of exercise, inhibits the NHE-1. We aim to explore the subcellular mechanisms involved in the heart and brain impact of physiological exercise in OVX rats. We speculate that physical training, via IGF-1, prevents the increase in ROS; improving heart and brain physiological functions during menopause. Exercise diminished cardiac ROS production and increased catalase (CAT) activity in OVX rats. In concordance, IGF-1 treatment reduces brain ROS, surely contributing to the improvement in brain behavior. Moreover, aerobic routine was able to prevent, and IGF-1 therapy to revert, NHE-1 hyperactivity in OVX rats. Finally, our results confirm the proposed signaling pathway as: IGF-1/PI3K-AKT/NO. Surprisingly, GPER inhibitor (G36) was able to abolish IGF-1 effect, suggesting that directly or indirectly GPER is part of IGF-1 pathway. We propose that IGF-1 is the main responsible for the protective effect of aerobic training both in heart and brain in OVX rats. Moreover, we showed that not only it is possible to prevent, but also to revert the menopause-induced NHE-1 hyperactivity by exercise/IGF-1 cascade. |
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2024 |
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2024-11-11 |
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