Prevention of Oxygen-Induced Inflammatory Lung Injury by Caffeine in Neonatal Rats

Figure 6

Hyperoxia exposure of newborn rat pups is characterized by modulation of cytokine response and regulation of redox-sensitive transcription factors. High oxygen led to increased proinflammatory cytokine expression of (a) TNFα (protein), (b) TNFα (RNA), (c) IL-1α, (d) IL-1β, and (e) IFNγ. Anti-inflammatory cytokine expression of (f) IL-10 is suppressed and redox-sensitive transcription factors (g) NFκB1 and (h) NFκB2 are increased. Caffeine counteracted this. Caffeine under normoxic exposure demonstrated a massive modulation of proinflammatory cytokine expression. Quantification of lung homogenates by qPCR for 3 days’ postnatal oxygen exposure (P3) and recovery (P3_P15) and 5 days’ postnatal oxygen exposure (P5) and recovery (P5_P15), respectively. Data are normalized to the level of rat pups exposed to normoxia at each time point (control 100%, white bars). The 100% values of TNFα protein are 4.4 (P3), 5.6 (P3_P15), 3.5 (P5), and 7.2 (P5_P15) pg per ml, respectively. -8/group (qPCR); /group (ELISA). , , , and vs. control; ^#, ^##, and ^#### vs. hyperoxia (ANOVA, Kruskal-Wallis, Dunn’s post hoc testq).