The JAK1-STAT1 signaling pathway triggers inflammation responses in chronic obstructive sleep apnea rat model
Fig 5
Correlation between JAK1-STAT1 activation and systemic inflammation.
(A) Positive correlation between p-STAT1 levels in lung tissues and serum IL-6 (r = 0.86, p < 0.001, Pearson correlation, n = 15). (B) Positive correlation between p-STAT1 levels and serum TNF-α (r = 0.82, p < 0.001, n = 15). (C) Airway resistance measured by forced oscillation at baseline and after methacholine challenge. Data are presented as mean ± SEM (n = 8 per group). Baseline resistance (open bars) did not differ among groups. Post-methacholine resistance (solid bars) was significantly elevated in the CIH group compared to the Sham group (***p < 0.001). Filgotinib treatment significantly attenuated this increase (###p < 0.001 vs. CIH group; one-way ANOVA with Tukey’s post hoc test). (D) Analysis of STAT3 pathway activation in lung tissues. Representative Western blot bands and quantitative analysis of total STAT3 and phosphorylated STAT3 (p-STAT3, Tyr705) protein levels in the Sham and CIH groups. β-actin was used as a loading control. Data are expressed as mean ± SEM (n = 8 per group). No statistically significant difference was found between the two groups (p > 0.05, unpaired t-test).