Specific Phase Expression Of Pax3and Cx43in Excessive Retinoic Acid Teratogenicity And Taurine Intervention On Neural Tube Defects

Objective To investigate the excess retinoic acid (RA) teratogenesis andtaurine intervention in the embryonic neural tube defects(NTDs), and analyze thePax3and Cx43specific phase expression in neural tube defects.Methods In this study, choosing healthy and virgin female Kunming mice andfeeding30mg/kg retinoic acid to this embryonic7.75days mice of one-time intragastric administration, in the deformity intervention group,let pregnant mices drink taurine2g/L water solution freely from E0,dealing the same as the deformity groupon E7.75, conventional breeding with food and water on the control group, fed withpure olive oil on E7.75;to fetal the neural tube defects and intervention animal models; each group have20female mices, cesareaning section at E9.5, E10.5, E11.5, E12.5respectively, using immunohistochemical methods and reverse transcription polymerase chain reaction analysis Pax3and Cx43specific phase expression in each group ofneural tube.Results (1)The encephalocele is the main deformity fetals in the teratogenicgroup, performance smaller than normal fetal in size, developmental lag, and itsoverall malformation rate reach to71.6%(189/264), stillbirth or absorbed embryorate is11.4%(34/298); Intervention group fetal rat performance calvarial closureinsufficiency, encephalocele is minor than teratogenic group, malformation ratewas significantly reduced compared with teratogenic is55.3%(152/275) P <0.05significant difference, the stillbirth or absorption of fetal rate is9.8%(30/305), the difference was not significant nature P>0.05,(2) Pax3protein and mRNAexpression in the neural tube: the positive reaction place of the Pax3proteinexpression is the nucleus, showed as brownish yellow. Pax3gene expression in thecontrol group was stronger than the two experimental groups (P <0.05), and thestrongest peak expression at E10.5; Pax3expression in the two experimentalgroups showing the increasing trend with embryo development, in the interventiongroup the Pax3expression is stronger than the teratogenic group (P <0.05).(3)Cx43protein and mRNA expression in the neural tube: Cx43protein positivereaction place is the cytoplasm and cell membrane, showed as brownish yellow.Cx43gene expression in the control group was weaker than the two experimentalgroups (P <0.05), and peak expression at E11.5; in the intervention group theexpression of Cx43was weaker than teratogenic group (P <0.05).Conclusion (1) This animal models of the teratogenicity of retinoic acidand intervention of taurine are stable and reliable, applies to the study of the NTDsanimal experiments.(2) Excessive retinoic acid caused Pax3and Cx43expressionphase disorder, reduced the Pax3expression, the expression peak disappear; and itenhanced the Cx43expression, causing fetal mouse NTDs, taurine can antagonizeretinoid teratogenic’s effects, improve the expression of the two genes, and reduceNTDs occur.(3) During the formation of NTDs, Pax3may be the negativeregulatory genes of Cx43.