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《Chinese Journal of Obstetrics and Gynecology》 2004-03
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Study of teratogenicity of hyperglycemia on neural tube defects and antagonistic effect of taurine

MAO Dong-wei *, ZHAO Yi-ping, LI Shou-rou, CHE Jian-hua, TAN Wen-hua. *Department of Obstetrics and Gynecology, The 211 Hospital of PLA, Ha′erbin 150080, China  
ObjectiveTo explore the molecular mechanism of neural tube defects (NTDs) caused by hyperglycemia and thiadiazole and the antagonistic effect of taurine MethodsThe pregnant mice were divided into hyperglycemia groups, thiadiazole group,taurine groups and control groups The mRNA and the protein of Pax3 or Cx43 gene were detected respectively by reverse transcription-polymerase chain reaction assay and immunohistochemical method ResultsAs compared with mice treated by thiadiazole-stomach-perfusing, NTDs were significantly increased from mice treated with glucose-injection when blood glucose levels were ≥ 13 4 mmol/L Elevated glucose and thiadiazole could cause changes in Pax3 and Cx43 expression Hyperglycemia had stronger developmental toxicity on mice embryos Expression of Pax3 (mRNA 0 97±0 20, protein 0 11±0 02) in hyperglycemia group was significantly decreased, while expression of Cx43 (mRNA 7 05±1 63, protein 0 94±0 05) was significantly increased, and the relationship of dose-effect was demonstrated In the thiadiazole group, the expression of Cx43 (mRNA 6 96±0 73, protein 0 92±0 12) was significantly stronger than control groups, but there were no significant differences in expression of Pax3 between thiadiazole and its control groups Both of their teratogenicity could be antagonized by taurine ConclusionsThis study suggests that congenital malformation associated with diabetic pregnancy is caused by disruption of regulatory genes,Pax3 and Cx43 expression in embryo in response to elevated glucose Thiadiazole can only disturb the regulation of Cx43 gene causing NTDs Taurine can correct the disruption caused by the two teratogens
【CateGory Index】: R715
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