摘要
目的研究褪黑素（MT）对细菌脂多糖（LPS）引起宫内胎儿死亡（IUFD）和生长发育迟缓（IUGR）的保护作用。方法实验1：LPS组小鼠于受孕第15-17天每天经腹腔注射LPS（75μg／kg），LPS＋MT组在LPS处理前和（或）处理后经腹腔注射MT，生理盐水和单纯MT处理作为对照。所有孕鼠于受孕第18天处死，统计活胎、死胎和吸收胎数，称量活胎体重，测量胎鼠身长和尾长，并对胎鼠骨骼发育情况进行评价。实验2：LPS组小鼠于受孕第16天经腹腔一次性注射75μg／kg LPS，LPS＋MT组孕鼠于LPS处理前和（或）处理后经腹腔注射MT，生理盐水和单纯MT处理作为对照。LPS处理后6h处死孕鼠，取母肝和胎盘，检测丙二醛和谷胱甘肽水平。结果LPS＋MT处理组宫内胎儿死亡数显著低于单纯LPS处理组，并呈明显剂量-效应关系；MT预＋后和后处理均显著减轻LPS引起生长发育迟缓，并逆转LPS引起的枕骨骨化不全。MT预＋后处理明显减轻LPS引起的母肝和胎盘脂质过氧化，但对LPS所致GSH含量降低无明显影响。结论MT通过其抗氧化功能保护LPS引起的IUFD和IUGR。
Objective To investiagate the effects of melatonin on LPS-induced intra-uterine fetal death （IUFD） and intra-uterine growth retardation （IUGR） in mice. Methods The present study included two separate experiments. Experiment 1, All pregnant mice except controls received an intraperitoneal injection of LPS （75 μg/kg, ip） on gd 15 - 17. The experiment was carried out in two different modes. In mode A, the pregnant mice received two doses of melatonin in 24 h, one （ 10 mg/kg, ip） injected immediately after LPS and the other （ 10 mg/kg, ip） injected at 3 h after LPS. In mode B, the pregnant mice were pretreated with 10 mg/kg of melatonin at 18 h before LPS and then received two doses of melatonin in 24 h, one （ 10 mg/kg, ip） injected immediately after LPS and the other （ 10 mg/kg, ip） injected at 3 h after LPS. The number of live fetuses, dead fetuses and resorption sites were counted on gd 18. Live fetuses in each litter were weighed. Crown-rump and tail lengths were examined and skeletal development was evaluated. Experiment 2, All pregnant mice except controls （ either saline or melatonin） received an intraperitoneal （75μg/kg） injection of LPS on gd 16. In mode A, the pregnant mice received two doses of melatonin, one （ 10 mg/kg, ip） injected immediately after LPS and the other （ 10 mg/kg, ip） injected at 3 h after LPS; In mode B, the pregnant mice were pretreated with 10 mg/kg of melatonin at 18 h before LPS and then received two doses of melatonin, one （ 10 mg/kg, ip） injected immediately after LPS and the other （ 10 mg/kg, ip） injected at 3 h after LPS. All dams were sacrificed at 6 h after LPS treatment. Maternal liver and placenta were dissected for GSH and MDA measurements. Results Post-treatment with melatonin significantly attenuated LPS-induced IUFD. Surprisingly, pre- plus post-treatments with melatonin almost blocked LPS-induced IUFD. In addition, both post-treatment and pre- plus post-treatments with melatonin significantly alleviated LPS-induced decreases in fetal weight and crown-rump and tail lengths, and reversed LPS-induced Supraoccipital boned developmental retardation. Furthermore, pre-plus post-treatments with melatonin significantly attenuated LPS-induced lipid peroxidation in maternal liver and placenta. However, melatonin had no effect on LPS-induced GSH depletion. Conclusion Melatonin protects against LPS -induced IURD and IUGR via counteracting LPS-induced oxidative stress.
出处
《安徽医科大学学报》
CAS
北大核心
2006年第4期368-371,共4页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金资助项目(编号:30371667
30572223)
安徽省自然科学基金资助项目(编号:050430714)
关键词
脂多糖类/毒性
褪黑激素/药理学
死胎
生长迟缓
lipopolysaccharides/toxicity
melatonin/pharmacology
fetal death
fetal growth retardation
