Fig. 1: Cardiac functions were compromised in prenatally DEX-exposed adult male offspring. | Cell Death & Disease

Fig. 1: Cardiac functions were compromised in prenatally DEX-exposed adult male offspring.

From: The detrimental effects of glucocorticoids exposure during pregnancy on offspring’s cardiac functions mediated by hypermethylation of bone morphogenetic protein-4

Fig. 1

a Diagram for the animal model procedure. Timed-pregnant mice at 14.5 dpc were injected subcutaneously with DEX (0.1 mg/kg/d) or NS at the same volume once a day until labor. Representative echocardiographic images of the adult male offspring prenatally exposed to NS (b) and DEX (c). The LVEF (d) and LVFS (e) were slightly but significantly decreased in the male offspring exposed to DEX during late gestation compared with that exposed to NS, which is NOT evident in female offspring. The LV dp/dt max and LV –dp/dt max in adult offspring did not show significant differences between NS group and DEX group before ischemia (f, h). The LV dp/dt max and LV –dp/dt max both significantly decreased after ischemia/reperfusion (I/R) injury in adult male offspring but not in adult female offspring, both prenatally exposed to DEX (g, i). NS, normal saline; DEX dexamethasone, LVEF left ventricular ejection fraction, LVFS left ventricular fractional shortening, dp/dt max maximal rate of left ventricle systolic pressure change, –dp/dt max maximal rate of left ventricle diastolic pressure change. Data shown are mean ± SEM. *p < 0.05, **p < 0.01

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