Effects of maternal PM_2.5 exposure during pregnancy on cardiovascular maldevelopment in rat offspring

Epidemiological studies suggest a link between maternal exposure to PM_2.5 during pregnancy and a higher incidence of fetal cardiovascular abnormalities. However, experimental data on the underlying mechanisms remain scarce.

This study aims to explore the effects of maternal PM_2.5 exposure during pregnancy on fetal cardiovascular maldevelopment in a rat model.

Twenty-eight pregnant rats were divided into control and PM_2.5-exposed groups according the exposure doses (N = 7 per group). Rats were administered with PM_2.5 suspensions corresponding to 0, 2.6, 5.5, and 11 μg/d, respectively, during gestation. On gestational day 21, neonatal hearts were collected, and levels of cardiac transcription factors (Tbx2, Tbx20, Hand2 and Gata6), MMP9, TN-C, VEGF-A, NF-κB, apoptotic markers (Bax/Bcl-2 ratio), catalase (CAT), and lipid metabolism indicators were measured.

In the 11 μg/d group, the mRNA levels of Tbx2, Tbx20, Hand2, Gata6, MMP9, TN-C and VEGF-A, the protein levels of Tbx2, Hand2, and TN-C, and blood CAT activity were significantly reduced (P < 0.05). Conversely, NF-κB, Bax/Bcl-2, and serum markers of dyslipidemia (TC, TG, LDH, LDL-C/HDL-C) were significantly elevated (P < 0.05). Additionally, TN-C and Hand2 mRNA levels were reduced in the 2.6 μg/d group, and LDH level was increased in the 5.5 μg/d group (P < 0.05).

Maternal PM_2.5 exposure during pregnancy is associated with fetal cardiovascular maldevelopments, possibly through the changes of cardiac transcription factors, vascular dysfunction, oxidative stress, apoptosis, and abnormalities of lipid metabolism.