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。
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 lag/kg, ip） daily on gestational 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, supraoccipital bone, caudal vertebrae, anterior and posterior phalanges, and metatarsus. Additional experinaent 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.
出处
《生殖与避孕》
CAS
CSCD
北大核心
2006年第8期456-460,共5页
Reproduction and Contraception
基金
国家自然科学基金(30371667
30572223)
安徽省自然科学基金(050430714)
