Fig. 1

High-altitude hypoxia induced increased levels of TNF-α, IL-1β, IL-6, and CRH in humans and rats. a Human SpO₂ was measured by fingertip pulse oximeter at low and high altitudes. b The levels of CRH in plasma of all human volunteers was determined by ELISA (n = 74). c The correlation between LLS score data and cytokines (TNF-α, IL-1β, and IL-6) level at high altitude by Spearman correlation analysis. d–f The levels of TNF-α, IL-1β, and IL-6 in plasma of all human volunteers was determined by ELISA (n = 74). ***P < 0.001 compared with control (low altitude, 540 m); ^# P < 0.05, ^### P < 0.001 compared with no-AMS group at high altitude (3860 m). g–i The rats in hypoxia group were exposed to hypoxia at altitude of 5000 min a hypobaric chamber for 2 days. The levels of CRH, TNF-α, and IL-1β in plasma were measured (n = 7). j, k Hypoxia-increased TNF-α and IL-1β levels in plasma were blocked by CRHR1 antagonist CP154,526 (n = 7). **P < 0.01; ***P < 0.001 compared with control, ^& P < 0.05 (hypoxia vs hypoxia + CRHR1 antagonist); the data are presented as mean ± SD