title: Antenatal supplementation of taurine for protection of fetal rat brain with intrauterine growth restriction from injury by reducing neuronal apoptosis.
abstract: This study aimed to investigate whether antenatal taurine can reduce neuronal apoptosis in fetal rat brains with intrauterine growth restriction (IUGR) and its possible mechanisms. A total of 15 pregnant rats were randomly divided into the following three groups: control, IUGR, and IUGR+ antenatal taurine supplements. Neuronal apoptosis was detected using transferase-mediated dUTP biotin nick end-labeling (TUNEL); the expression of Bcl-2, Bax, and caspase-3 mRNA and proteins was detected by reverse transcription-polymerase chain reaction and immunohistochemistry. In IUGR groups, the results were as follows: (1) the expression of Bcl-2 decreased whereas the expression of Bax increased, accordingly, the ratio of Bcl-2/Bax decreased, (2) the expression of caspase-3 increased significantly, and (3) apoptotic neuron counts in IUGR groups was significantly increased compared with controls. In taurine supplement groups, the results were as follows: (1) the expression of Bcl-2 increased whereas the expression of Bax decreased, accordingly, the ratio of Bcl-2/Bax increased, (2) the expression of caspase-3 in fetal rat cerebral cortex tissues decreased significantly, and (3) the number of apoptotic neurons was significantly decreased compared with IUGR groups. In addition, the changes in the expression of Bcl-2, Bax, and caspase-3 mRNA and protein were correlated. So we concluded that antenatal supplementation of taurine may reduce neuronal apoptosis in IUGR fetal rats via up-regulating the ratio of Bcl-2/Bax and down-regulating the expression of caspase-3.
authors.affiliation: Department of Neonatology and NICU of Bayi Children's Hospital, General Hospital of Beijing Military Command, Beijing, China. Liujingbj@live.cn
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Liu
authors.forename: Xiao-Feng
authors.initials: XF
authors.lastname: Wang
authors.forename: Hui-Yun
authors.initials: HY
authors.lastname: Teng
authors.forename: Na
authors.initials: N
authors.lastname: Yang
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D029681:Arabidopsis Proteins / Q000378:metabolism; D001921:Brain / Q000473:pathology*; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000473:pathology / Q000517:prevention & control*; D020287:In Situ Nick-End Labeling / Q000379:methods; D066298:In Vitro Techniques; D019751:Intramolecular Transferases / Q000378:metabolism; D009474:Neurons / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000008:administration & dosage*; D011247:Pregnancy; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000008:administration & dosage*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D029681:Arabidopsis Proteins; C494828:Bax protein, rat; D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D013654:Taurine; C505409:Casp3 protein, mouse; D053148:Caspase 3; D019751:Intramolecular Transferases; C568454:marneral synthase, Arabidopsis