Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress.
hypertension
kinin B1 receptor
neuroinflammation
neurons
oxidative stress
Journal
Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981
Informations de publication
Date de publication:
08 Jan 2023
08 Jan 2023
Historique:
received:
19
12
2022
revised:
03
01
2023
accepted:
05
01
2023
entrez:
21
1
2023
pubmed:
22
1
2023
medline:
22
1
2023
Statut:
epublish
Résumé
Hypertension is associated with increased expression of kinin B1 receptors (B1R) and increased levels of pro-inflammatory cytokines within the neurons. We previously reported that angiotensin II (Ang II) upregulates B1R expression and can induce neuroinflammation and oxidative stress in primary hypothalamic neurons. However, the order in which B1R activation, neuroinflammation, and oxidative stress occur has not yet been studied. Using primary hypothalamic neurons from neonatal mice, we show that tumor necrosis factor (TNF), lipopolysaccharides (LPS), and hydrogen peroxide (H
Identifiants
pubmed: 36671012
pii: antiox12010150
doi: 10.3390/antiox12010150
pmc: PMC9854481
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL153115
Pays : United States
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