Ontology highlight
ABSTRACT: Background
Chronic obstructive sleep apnea (OSA) drives systemic inflammation; the role of the JAK1-STAT1 pathway is unclear.Objective
To elucidate JAK1-STAT1 involvement in OSA-related inflammation using a chronic intermittent hypoxia (CIH) model.Methods
Sprague-Dawley rats underwent 8-week CIH (FiO₂ cycling 5-21%, 8h/day) or normoxia (Sham). Serum cytokines (ELISA) and lung p-JAK1/p-STAT1 (Western blot/IHC) were analyzed. A CIH subset received JAK1 inhibitor filgotinib. Airway resistance was assessed via forced oscillation.Results
CIH elevated serum IL-6/TNF-α versus Sham (p < 0.05) and increased lung p-JAK1/p-STAT1. Filgotinib reduced cytokines, suppressed p-JAK1/p-STAT1, attenuated leukocyte infiltration/collagen deposition, and improved airway resistanc
SUBMITTER: Yang L
PROVIDER: S-EPMC12912577 | biostudies-literature | 2026
REPOSITORIES: biostudies-literature