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

Figure 2

Quantitative analysis of (a) DFFB+ cell counts showed a marked increase in lung tissue samples of rat pups after acute oxygen exposure at P3 and P5 (deep dark grey bars) whereas caffeine treatment reduced apoptotic cells (dark grey bars). Cell death rate remained elevated even after recovery (P15). Caffeine treatment under room air (light grey bars) demonstrated no modulation of cell death. Hyperoxia within the first days of life accompanied by an increased cell death rate led to enhanced gene expression of (b) Casp3, (c) GCLC, and (d) AIF. Caffeine counteracted this. Quantification of lung homogenates was performed with 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), and the 100% values are 4.3 (P3), 1.7 (P3_P15), 3.1 (P5), and 0.7 (P5_P15) cells per mm², respectively. -8/group. , , , and vs. control; ^#, ^##, and ^#### vs. hyperoxia (ANOVA, Kruskal-Wallis, Dunn’s post hoc test).