Abstract

Objective To determine the optimal timing of antenatal taurine supplementation to improve neuron and neural stem cell proliferation in fetal rats with intrauterine growth restriction. Methods Twenty-five pregnant SD rats were randomly divided into five groups (five rats in each group): group A was the control group, group B to E were the fetal growth restriction (FGR) model groups with low-protein diet during the experiment, group C, D, and E were supplemented with taurine [300 mg/(kg·d)] at day 9, 11 and 15, respectively. The birth weight of newborn rats was measured after natural delivery. The rats with body weight two standard deviations lower than the average weight in group A were diagnosed as FGR. There were five litters of newborn rats in each group, and two were randomly selected from each litter, resulting in ten newborn rats in each group. Proliferating cell nuclear antigen (PCNA) and fatty acid binding protein 7 (FABP7) positive cell expression in newborn rat brain tissues were detected by immunohistochemistry. Single factor analysis of variance, LSD tests were used for statistical analysis. Results The average birth weight of newborn rats in group A, B, C, D and E were (6.61±0.45), (4.65±0.23), (5.37±0.17), (5.74±0.21), and (5.00±0.24) g, respectively. Average birth weight was lower in group B than in group A (t=2.447), higher in group D and E than in group B (t=2.306 and 2.306), higher in group D than in group C and E (t=2.306 and 2.306), and the differences were statistically significant (all P 0.05). The IOD in group D was higher than that in group E, and the difference was statistically significant (t=4.182, P<0.05). Conclusions Antenatal taurine supplementation can promote neuron and neural stem cell proliferation in rats with FGR. The effect is most obvious on the 11th day of pregnancy, and may lead to the promotion of brain development. Key words: Fetal growth retardation; Taurine; Neurons; Neural stem cells; Cell proliferation; Proliferating cell nuclear antigen; Nerve tissue proteins; Fatty acid-binding proteins; Disease models, animal

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