中文摘要：

目的研究抗坏血酸（AA）对细菌脂多糖（LPS）引起宫内胎儿死亡（IUFD）、生长发育迟缓（IUGR）和骨骼发育迟缓的保护作用。方法实验1：LPS组小鼠于妊娠第15～17d经腹腔注射LPS，LPS＋AA组在LPS处理前和／或处理后经腹腔注射给予AA，对照组给予等容量的生理盐水或从。所有孕鼠于妊娠第18d处死。实验2：LPS组小鼠于妊娠第16d注射LPS，LPS＋AA组在LPS处理前和／或处理后经腹腔注射给予AA，对照组给予等容量的生理盐水或AA。LPS处理后6h处死孕鼠。结果LPS＋AA预处理组平均每窝死胎数明显低于单纯LPS处理组，LPS＋从后和预＋后处理组平均每窝死胎数与单纯LPS组比较差异无统计学意义；AA预、后和预＋后处理均显著抑制LPS引起IUGR和枕骨骨化不全。从预和后处理均显著抑制LPS引起母肝、胎肝和胎盘组织脂质过氧化。但从预处理的作用强于后处理。结论从预处理通过抑制LPS引起的氧化应激，预防LPS引起IUFD、IUGR和骨骼发育迟缓；AA后处理和预＋后处理对抗LPS引起IUGR和骨骼发育迟缓，但对LPS引起的IUFD无明显保护作用。

英文摘要：

Objective To investigate the effects of ascorbic acid （AA） on lipopolysaccharide（LPS）-induced intra-uterine fetal death （IUFD）, intra-uterlne growth retardation （IUGR） and skeletal development retardation in mice. Methods Experiment 1 ：all pregnant mice except controls （either saline or AA） received an intraperitoneal （75 μg/kg, ip） injection of LPS on gd 15- 17. In LPS ＋ AA groups, the pregnant mice were treated with AA at 0.5 h before LPS and/or 3 h after LPS. All dams were sacrificed on gd 18. Experiment 2 ：all pregnant mice except controls （either saline or AA） received an intraperitoneal （75μg/kg, ip） injection of LPS on gd 16. In LPS ＋ AA groups, the pregnant mice were treated with AA at 0.5 h before LPS and/or 3 h after LPS. All dams were sacrificed at 6 h after LPS. Results Pretreatment with AA significantly attenuated LPS-indueed lipid peroxidatlon, decreased fetal mortality, and reversed LPS-induced fetal growth and skeletal development retardation. However, post-treatment with AA had less effect on LPS-induced IUFD, although post-treatment significantly attenuated LPS-induced lipid peroxidation and reversed LPS-induced fetal growth and skeletal development retardation. Furthermore, post-treatment with AA reduced the protective effects of pretreatment on LPS-induced IUFD. Conclusion Pretreatment with AA protected against LPS-induced fetal death and reversed LPS-induced growth and skeletal developmen tretardation via counteracting LPS-induced oxidative stress, whereas post-treatment and pre- ＋ post-treatment had less effect on LPS-induced IUFD.