| Purpose:Prenatal exposure to air pollution is associated with negative outcomes in the offspring of newborns and adults.Literature and our previous studies demonstrated epidemiologically and experimentally that atmospheric inhalable particles(PM10)can cause fetal cardiovascular malformations.While,fine particulate matters(PM2.5)in PM10 can enter the blood system through the pulmonary blood-air barrier,which can further affect the development of fetus directly or indirectly by affecting the mother and placenta,causing greater damage to human body.Our previous studies have also shown that PM2.5 can cause damage to mouse ovaries and embryos,however,the effect of PM2.5 on fetal heart development and its mechanisms need to be further investigated.Methods:In this study,we first prepared local PM2.5 suspensions at different concentrations,and randomly divided 40 female SD rats into 5 groups(n=8):The control group,0.26,0.55,1.10 and 3.68μg/μl PM2.5 expose groups.Rats in each exposed group were given intratracheal instillation of PM2.5 suspensions,once every 3 days,and the 3-day dose was given in one time with a total of 30μl liquid.The control group was given the same amount of carboxymethylcellulose sodium solution.The administration period included 30 days before conception(gametic development)till 21 days after conception(intrauterine development).At day 21 of gestation,the rats were allowed to deliver naturally or their fetuses retrieved by laparotomy alternatively.A dam from 1.10 or 3.68μg/μl PM2.5 exposed group was selected for pulmonary light microscopy.The hearts of newborn rats were examined by transmission electron microscopy,protein and mRNA levels for plasma TNF-α and IL-6 were examined by ELISA,and cardiac transcription factors MEF2C and TBX5 protein and mRNA levels were examined by western-blotting and qPCR,respectively.Result:With the increase of PM2.5 exposure concentrations,injuries in myofibrin and mitochondria were increasingly worsen with the amount of glycogen particles decreased.Lysosomes and apoptotic bodies were observed in the 3.68μg/μl group.Myocardial cell apoptosis and plasma inflammatory factors were obviously increased with the increase of exposure concentrations.Compared with the corresponding control group,the mRNA expression levels of MEF2C in the heart tissue of the newborn rats were significantly decreased in all the exposed groups,and the mRNA expression levels of TBX5 were significantly lower in 0.26,0.55 and 1.10μg/μl groups but significantly higher in 3.68μg/μl group(Pall<0.05).The protein contents of MEF2C in 0.55 and 1.10μg/μl groups and of TBX5 in 026,0.55 and 1.10μg/μl groups were increased significantly versus their corresponding control group(P<0.05).There was no significant difference for MEF2C or TBX5 protein level between the 3.68μg/μl group and control group(Pall>0.05).Conclusion:Our data shows that prenatal exposure to PM2.5 pollution can elicit adverse effects on fetal cardiac development by damaging cardiomyocytes,causing inflammatory responses and altering the expression of important transcription factors of heart development. |
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