【摘要】 目的:研究细菌脂多糖(LPS)对小鼠宫内胎儿死亡(IUFD)、生长发育迟缓(IUGR)和骨骼发育迟缓的影响。方法:LPS低中高组小鼠于妊娠d15-17分别腹腔注射不同剂量LPS(25μg/kg、50μg/kg、75μg/kg),LPS+2-苯叔丁基硝酮(PBN,活性氧ROS拮抗剂)组在LPS(75μg/kg)处理前30min和后3h经腹腔各给予100mg/kg的PBN,对照组给予等容量生理盐水。孕鼠于妊娠d18处死。另给药1d时取LPS高剂量组LPS+PBN组和对照组于LPS处理后6h处死孕鼠。结果:①小鼠妊娠d15-17给予LPS后,中高剂量组平均每窝死胎数明显高于对照组,活胎体重、身长和尾长下降,并呈明显的剂量-效应关系;LPS高剂量导致IUGR和骨骼发育迟缓;PBN处理明显抑制LPS对胎儿的作用。②LPS使母肝、胎肝和胎盘组织脂质过氧化,GSH含量显著降低。PBN显著抑制LPS的这些作用。结论:母鼠妊娠晚期接触LPS引起IUFD、IUGR和骨骼发育迟缓,ROS至少部分参与了LPS的引起IUFD、IUGR和骨骼发育迟缓。更多还原

【Abstract】 Objective:To investigate the effect of Lipopolysaccharide(LPS)on intra-uterine fetal death(IUFD),fetal growth retardation(IUGR)and skeletal development retardation in mice.Methods:In experiment 1:Pregnant mice except controls(saline)were injected with different doses of LPS(25-75 μg/kg,ip)daily on gesta-tional day 15-17.In LPS+PBN group,pregnant mice were treated with N-tert-butyl-α-phenylnitrone(PBN)at 30 min before LPS and 3 h after LPS.All mice were sacrificed on day 18.In experiment 2:All pregnant mice except controls(saline)received an intraperitoneal(75 μg/kg,ip)injection of LPS on d 15.In LPS+PBN group,the pregnant mice were treated with PBN at 30 min before LPS and 3 h after LPS.All mice were sacrificed at 6 h after LPS.Results:Maternal LPS exposure resulted in IUFD,and significantly decreased fetal weight and crown-rump and tail lengths of live fetuses in a dose-dependent manner.LPS retarded skeletal ossification in sternum,supraoc-cipital bone,caudal vertebrae,anterior and posterior phalanges,and metatarsus.Additional experiment showed that LPS significantly increased MDA level and decreased GSH content in maternal liver,fetal liver and placenta.PBN significantly attenuated LPS-induced lipid peroxidation in maternal liver,fetal liver and placenta.Consistent with its antioxidative effect,PBN blocked LPS-induced IUFD and reversed LPS-induced growth and skeletal development retardation.Conclusion:Maternal LPS exposure results in IUFD,IUGR and skeletal development retardation in mice.Reactive oxygen species(ROS)are,at least in part,mediated in LPS-induced IUFD,IUGR and skeletal development retardation.更多还原