Analysis of Nuclear Erythroid Factor 2 in Vascular Reactivity of Spontaneously Hypertensive Rats Treated With Apocynin

  • Autor
  • Andrea Estéffane Soares Cardoso de Oliveira
  • Co-autores
  • Murilo Eduardo Graton , Jéssica Luiza de Oliveira Fonseca Zanardo , Cristina Antoniali Silva
  • Resumo
  • Introduction: Reactive oxygen species imbalance generates oxidative stress, resulting in chronic diseases, such as high blood pressure (BP). In order to neutralize it, cells synthesize antioxidant enzymes, for example, Nuclear factor erythroid 2-related factor 2 (Nrf-2). A molecule called apocynin (APO) reduces oxidative stress and vascular damage. Objective: Analyze Nrf-2’s role in aortas of Wistar and Spontaneously Hypertensive Rats (SHR) treated or not with APO. Methods: SHR (n=4) and Wistar (n=6) male rats, from 4th-10th week post-natal, were treated with APO (30mg/Kg/day,vo); control group composed by SHR (n=7) and Wistar (n=5) (CEUA0855-2017). On the 10th week, SHR (300g) and Wistar (450g) had their thoracic aortas removed, after euthanasia by decapitation, utilzing isoflurane as anesthesic. They were cut into 2-mm rings and positioned in the vascular reactivity measurement apparatus (DMT, ADInstruments, Australia) with Krebs-Henseleit solution. Results: APO reduced BP, increased contractions of aortas exposed to Phenylephrine (PE) and shifted the concentration-effect curves in response to Acetylcholine (ACh) to the right. Brusatol did not change the reactivity of aortas exposed to untreated PE or ACh from SHR, but shifted PE curves to the right and ACh curves to the left in SHR aortas treated with apocynin. APO-treated Wistar aortas were more reactive to PE compared to untreated Wistar. Brusatol increased the contractions of the concentration-effect curves for PE in untreated Wistar, but did not change the reactivity of APO-treated ones; in these rats, APO does not promote changes in endothelial, as vasodilator responses to ACh depend of the presence of the endothelium and eNOS activity. Conclusion: APO modified responses to PE, ACh and the role of Nrf-2 in SHR, and it also modified responses to PE in Wistar, however our data also suggests that ACh's vasodilator response in Wistar does not depend on Nrf-2 activity. 

  • Palavras-chave
  • Apocynin, Nrf-2, blood pressure
  • Modalidade
  • Pôster
  • Área Temática
  • Inflamação e doenças vasculares
Voltar
  • Estresse oxidativo
  • Disfunção endotelial
  • Produtos naturais
  • Inflamação e doenças vasculares
  • Sinalização celular
  • Tecido adiposo perivascular
  • Sistema endócrino e doenças vasculares
  • Revisões, projetos, revisões sistemáticas e metanálises em biologia vascular
  • Educação em saúde e doenças vasculares
  • COVID-19 e complicações vasculares

Comissão Organizadora

José Wilson do Nascimento Corrêa
Simone Potje
Gabriel Tavares do Vale
Stêfany Cau
Roger Lyrio
Simone R Potje
Alice Valença Araújo
Ruth Cristina Albuquerque Santos
Lara Caroline Amaro
Ana Dária Cassoli da Silva
Pollyana Peixoto
Izabela Moreira Bonfim
Jocimar José Pitol
Sunamita Vaz Martins
Izabela Moreira Bonfim
Palloma Emanuelle Dornelas de Melo
Daniella Bonaventura
Tagana Rosa
Sarah Victory Santana Gomes
Priscila Cruz
André Lucas Borges
Jéssyca Aparecida Soares Giesen
Leticia Tinoco Gonçalves
Silvia Maria Luna Alves
NAYANA YARED BATISTA
Wellington Francisco Pereira da Silva
Natália Ferreira de Araújo
Leandro de Carvalho Gomes

Comissão Científica