Objective To investigate the effects of preconception exposure to fine particulate matter (PM_2.5) on the cardiac function of offspring adult mice and its underlying mechanism.

Methods Twenty-eight 8-week-old female C57BL/6J mice were randomly divided into control group and PM_2.5 exposure group, with 14 mice per group. The exposure group received intranasal infusion of a PM_2.5 suspension at 3 mg/kg, while the control group received a suspension treated with a blank sampling membrane, once every two days for four weeks. At the end of the exposure, the female mice in each group were caged with normal male mice overnight at a ratio of 2:1, and the presence of vaginal plugs on the next morning indicated the occurrence of pregnancy. The offspring of the two groups were fed and monitored for body weight until the 10th week. Six mice were examined for cardiac function, 3 mice were examined for pathological changes on heart slices, and 4 mice were examined for the mRNA expression levels of the hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway and angiogenesis markers, including platelet-endothelial cell adhesion molecule (CD31), angiopoietin-1, and von Willebrand factor(vWF).

Results Compared with the control group, preconception PM_2.5 exposure had a significant inhibitory effect on the body weight of offspring mice (post-natal day 7). Offspring adult of the exposure group showed significantly increased left ventricular mass(LVM), left ventricular end-diastolic anterior wall thickness (LVAW-d), and left ventricular end-diastolic posterior wall thickness(LVPW-d); significantly decreased systolic parameters of left ventricular ejection fraction(EF), left ventricular fractional shortening(FS), and stroke volume(SV); significantly increased diastolic parameter (isovolumic contraction time, IVRT) and myocardial function parameter (Tei); and pathological changes including heart enlargement, inflammatory cell infiltration, and vascular abnormalities. Further molecular analysis showed that preconception PM_2.5 exposure could affect the angiogenesis of offspring adult mice.

Conclusion Preconception PM_2.5 exposure may interfere with angiogenesis through the HIF-1α/VEGF signaling pathway, subsequently affecting the cardiac function of offspring adult.