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Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation

Rudgea viburnoides is widely found in the Brazilian Cerrado, and commonly used in Brazilian folk medicine. In this study, we evaluated the effects of prolonged administration of the aqueous extract from R. viburnoides leaves (AERV) on impaired redox status, renal dysfunction, and cardiovascular dama...

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Autores principales: Paulin, Fernanda Viana, Palozi, Rhanany Alan Calloi, Lorençone, Bethânia Rosa, Macedo, Arthur Ladeira, Guarnier, Lucas Pires, Tirloni, Cleide Adriane Signor, Romão, Paulo Vitor Moreira, Gasparotto Junior, Arquimedes, Silva, Denise Brentan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8537958/
https://www.ncbi.nlm.nih.gov/pubmed/34683872
http://dx.doi.org/10.3390/pharmaceutics13101579
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author Paulin, Fernanda Viana
Palozi, Rhanany Alan Calloi
Lorençone, Bethânia Rosa
Macedo, Arthur Ladeira
Guarnier, Lucas Pires
Tirloni, Cleide Adriane Signor
Romão, Paulo Vitor Moreira
Gasparotto Junior, Arquimedes
Silva, Denise Brentan
author_facet Paulin, Fernanda Viana
Palozi, Rhanany Alan Calloi
Lorençone, Bethânia Rosa
Macedo, Arthur Ladeira
Guarnier, Lucas Pires
Tirloni, Cleide Adriane Signor
Romão, Paulo Vitor Moreira
Gasparotto Junior, Arquimedes
Silva, Denise Brentan
author_sort Paulin, Fernanda Viana
collection PubMed
description Rudgea viburnoides is widely found in the Brazilian Cerrado, and commonly used in Brazilian folk medicine. In this study, we evaluated the effects of prolonged administration of the aqueous extract from R. viburnoides leaves (AERV) on impaired redox status, renal dysfunction, and cardiovascular damage in 2K1C hypertensive rats, as well as its chemical composition by LC-DAD-MS. Renal hypertension (two kidney, one-clip model) was surgically induced in male Wistar rats and AERV (30, 100 and 300 mg/kg) was administered orally five weeks after surgery for 28 days. Renal function was assessed and urinary electrolytes, pH, and density were measured. Electrocardiography, blood pressure and heart rate were recorded. Cardiac and mesenteric vascular beds were isolated for cardiac morphometry and evaluation of vascular reactivity, and aortic rings were also isolated for measurement of cyclic guanosine monophosphate levels, and the redox status was assessed. Prolonged treatment with AERV preserved urine excretion and electrolyte levels (Na(+), K(+), Ca(2+) and Cl(−)), reversed electrocardiographic changes, left ventricular hypertrophy and changes in vascular reactivity induced by hypertension, and reduced blood pressure and heart rate. This effect was associated with a positive modulation of tissue redox state, activation of the NO/cGMP pathway, and inhibition of the angiotensin-converting enzyme. Glycosylated iridoids, chlorogenic acids, glycosylated triterpenes, O-glycosylated flavonols, and triterpenoid saponins were annotated. AERV showed no acute toxicity in female Wistar rats. Therefore, AERV treatment reduced the progression of cardiorenal disease in 2K1C hypertensive rats, which can be involved with an important attenuation of oxidative stress, angiotensin-converting enzyme inhibition, and activation of the NO/cGMP pathway.
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spelling pubmed-85379582021-10-24 Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation Paulin, Fernanda Viana Palozi, Rhanany Alan Calloi Lorençone, Bethânia Rosa Macedo, Arthur Ladeira Guarnier, Lucas Pires Tirloni, Cleide Adriane Signor Romão, Paulo Vitor Moreira Gasparotto Junior, Arquimedes Silva, Denise Brentan Pharmaceutics Article Rudgea viburnoides is widely found in the Brazilian Cerrado, and commonly used in Brazilian folk medicine. In this study, we evaluated the effects of prolonged administration of the aqueous extract from R. viburnoides leaves (AERV) on impaired redox status, renal dysfunction, and cardiovascular damage in 2K1C hypertensive rats, as well as its chemical composition by LC-DAD-MS. Renal hypertension (two kidney, one-clip model) was surgically induced in male Wistar rats and AERV (30, 100 and 300 mg/kg) was administered orally five weeks after surgery for 28 days. Renal function was assessed and urinary electrolytes, pH, and density were measured. Electrocardiography, blood pressure and heart rate were recorded. Cardiac and mesenteric vascular beds were isolated for cardiac morphometry and evaluation of vascular reactivity, and aortic rings were also isolated for measurement of cyclic guanosine monophosphate levels, and the redox status was assessed. Prolonged treatment with AERV preserved urine excretion and electrolyte levels (Na(+), K(+), Ca(2+) and Cl(−)), reversed electrocardiographic changes, left ventricular hypertrophy and changes in vascular reactivity induced by hypertension, and reduced blood pressure and heart rate. This effect was associated with a positive modulation of tissue redox state, activation of the NO/cGMP pathway, and inhibition of the angiotensin-converting enzyme. Glycosylated iridoids, chlorogenic acids, glycosylated triterpenes, O-glycosylated flavonols, and triterpenoid saponins were annotated. AERV showed no acute toxicity in female Wistar rats. Therefore, AERV treatment reduced the progression of cardiorenal disease in 2K1C hypertensive rats, which can be involved with an important attenuation of oxidative stress, angiotensin-converting enzyme inhibition, and activation of the NO/cGMP pathway. MDPI 2021-09-28 /pmc/articles/PMC8537958/ /pubmed/34683872 http://dx.doi.org/10.3390/pharmaceutics13101579 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Paulin, Fernanda Viana
Palozi, Rhanany Alan Calloi
Lorençone, Bethânia Rosa
Macedo, Arthur Ladeira
Guarnier, Lucas Pires
Tirloni, Cleide Adriane Signor
Romão, Paulo Vitor Moreira
Gasparotto Junior, Arquimedes
Silva, Denise Brentan
Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation
title Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation
title_full Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation
title_fullStr Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation
title_full_unstemmed Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation
title_short Prolonged Administration of Rudgea viburnoides (Cham.) Benth. Prevents Impairment of Redox Status, Renal Dysfunction, and Cardiovascular Damage in 2K1C-Hypertensive Rats by Inhibiting ACE Activity and NO-GMPC Pathway Activation
title_sort prolonged administration of rudgea viburnoides (cham.) benth. prevents impairment of redox status, renal dysfunction, and cardiovascular damage in 2k1c-hypertensive rats by inhibiting ace activity and no-gmpc pathway activation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8537958/
https://www.ncbi.nlm.nih.gov/pubmed/34683872
http://dx.doi.org/10.3390/pharmaceutics13101579
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