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At present, the mouse model of congenital heart disease is mainly constructed, using C57BL/6J mice, but the C57BL/6J mouse model of conotruncal cardiac defects has not been successfully established. The objective is to explore optimal method to induce conotruncal cardiac defects with all-trans retinoic acid, providing the basis for establishment of transgene animal model.
68 pregnant C57BL/6J mice at 8 weeks of age were divided into 2 groups: Control group (n=8), the mice received a single dose of Dimethyl Sulphoxide (DMSO) at 8.5 days of gestation by gavage, and Experiment group (n=60), the mice were divided into 3 subgroups, received a single dose of all-trans retinoic acid, 45mg/kg, 50mg/kg and 55mg/kg respectively at 8.5 days of gestation by gavage. All animals were treated for 18.5 days and then the embryos were taken to observe cardiac morphology under stereomicroscope and checked by H&E staining.
Compared with Control group, Experiment group had obviously increased occurrence rates of abortion and embryo absorption, and 95.9% phenotype for conotruncal cardiac defects. Experiment group also had non-cardiac defective phenotypes, including exophthalmos, exomphalos, spinal malformation et al. Low concentration group (45mg/kg) had 65.0% normal cardiac phenotype, 35.0% Conotruncal Cardiac Defects (double outlet of right ventricle, transposition of great arteries and persistent truncus arteriosus); middle and high concentration group (50-55mg/kg) contained 22.2% normal cardiac phenotype, 77.8% Conotruncal Cardiac Defects.
All-trans retinoic acid may induce conotruncal cardiac defects in C57BL/6J mice embryos and concentration gradient has effect on conotruncal defective phenotype.