The Conflicting Role of Caffeine Supplementation on Hyperoxia-Induced Injury on the Cerebellar Granular Cell Neurogenesis of Newborn Rats

Figure 7

Quantification of cerebellar homogenates for granule cell precursor- and/or Purkinje cell-associated mediators of (a) BDNF, (b) Calb1, and (c) Shh 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. Acute hyperoxia exposure (deep dark gray bars) decreased the mRNA expression at P3 and/or P5, except for BDNF with an increase at P5. At P15, the reduction of Calb1 persisted after three-day oxygen exposure (P3_P15), or the reduction of BDNF, Calb1, and Shh evolved after five-day oxygen exposure (P5_P15). Caffeine most antagonized hyperoxia-induced effects (gray bars) after recovery for BDNF and Shh at P5_P15 but reduced the overexpressed levels of BDNF at P5. Caffeine with normoxia (light gray bars) modulated the expression levels in a more differential manner. Data are normalized to the level of rat pups exposed to normoxia at each time point (control 100%, white bars). -8/group. , , , and vs. control;^## and ^### vs. hyperoxia (ANOVA, Bonferroni’s post hoc test; Kruskal-Wallis, Dunn’s post hoc test; Brown-Forsythe, Dunnett’s post hoc test).