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The Experimental Animal Study Of NTDs Induced By All-trans Retinoic Acid In C57 Mouce

Posted on:2013-05-28Degree:MasterType:Thesis
Country:ChinaCandidate:R WuFull Text:PDF
GTID:2234330371977345Subject:Biochemistry and Molecular Biology
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ObjectiveTo study the NTDs induced by all-trans retinoic acid (ATRA) in different quantity and different effected time in C57mouce.MethodsTreatment of C57pregnant mice with different doses of all-trans retinoic acid on E7.5day with pina bifida, embryos were gained on E11.5day. The embryos without extraembryonic membranes were being histological section and HE colorated observation, and detected apoptosis happened. To examine whether in vivo administration of Z-VAD-FMK would prevent infection-induced preterm-delivery.ResultsIn our study, treatment was commenced on the optimal concertration RA,21mg/kg. The control was normal. In the E7.5d group brain growth was sluggish, and brain abnormality was happened and the ratio of malformation was100%, the ratio of absorbing fetus was27%. In the E8.25d group, spina bifida was the main abnormality and the ratio was84%, brain abnormality was a few, absorbing fetus was27%. In the HE colorated experiment, the wall of neural tube was normal, configuration was full and mesenchymal cell distributed equably in the control, and in the experiment group, the quantity of cell were reduced, the wall were thinner. Most apoptosis cells were found around vertebra of rat embryo but a little were found in normal by TUNEL cell coloration detection. When worked on the pragnent rats which being pretreatment by the apoptosis inhibitor Z-VAD-FMK, the less happened in neural tube abnormality.ConclusionsNTDs mouse model of C57breed was successfully built induced by ATRA, which makes perfect model foundation for the study of pathogeny of NTDs. We also found that in vitro treatment with pancaspase inhibitor Z-VAD-FMK protects trophoblasts from microbial antigen-induced apoptosis.
Keywords/Search Tags:All-trans-retinoic acid(ATRA), neural tube defects(NTDs), animal model, apoptosis
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