Figure 4
From: Prevention of neonatal oxygen-induced brain damage by reduction of intrinsic apoptosis

TRP601 treatment inhibits hyperoxia-induced intrinsic apoptosis. (a) Western blot analysis from thalamic cytosolic and mitochondrial protein fractions implies a shift of cytochrome c from mitochondria to the cytosol under hyperoxic conditions that could be prevented by a single TRP601 treatment (1 mg/kg, i.p.). (b) Western blot analysis of Apaf-1 expression in thalamic brain samples displays a significant upregulation after 12 and 24 h hyperoxia, which was blocked by TRP601. The densitometric data represent the density ratio of relevant individual bands to the corresponding internal standard band (β-actin or VDAC). Data are normalized to levels of rat pups exposed to normoxia (control 100%; bars represent mean±S.E.M., n=6/group, ***P<0.001, ###P<0.001, one-way ANOVA compared with respective controls). Blots are representative of a series of three blots