Fig. 1: Misoprostol prevents hypoxia-induced contractile and mitochondrial dysfunction in vivo.

A Schematic of the mouse model of neonatal hypoxia, where mice are exposed to hypoxia (10% O₂) with or without 10 μg/kg misoprostol daily from PND3-10. B Fractional shortening, (C) Ejection fraction, and (D) E’/A’ ratio, for 4-6 post-natal day (PND10) mice treated as in (A), as determined by transthoracic echocardiography. E PCR-based array performed on RNA isolated from PND10 mouse ventricles (n = 3 animals per group) treated as in (A), where green indicates a downregulation of expression (<1), and red indicates an upregulation of expression (>1), relative to the normoxic control (1). F Measurement of ATP content in PND10 mouse ventricles (n = 6–8 animals per condition) treated as in (A). G Measurement of cardiac lactate content in the PND10 mouse ventricle (n = 6–8 animals per condition) treated as in (A). H PND10 hearts treated as in (A) and imaged via transmission electron microscopy. Images showing mitochondrial morphology. I PND10 hearts treated as in (A) and stained with DAPI (Blue) and probed for high mobility group box 1 (HMGB1, red). Hearts were imaged via confocal microscopy. J Representative immunoblot of heart protein extracts from post-natal day (PND10) mice treated as in (A). Extracts were immunoblotted as indicated. K Relative Bnip3 gene expression from the PND10 mouse ventricles of animals (n = 6–9 animals per group) treated as in (A). All data are represented as mean ± S.E.M. *P < 0.05 compared with control, while **P < 0.05 compared with hypoxia treatment, determined by 1-way ANOVA or 2-way ANOVA where appropriate. Three * indicates P < 0.05 compared to both control and treatment conditions.