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陈远华, 徐德祥, 赵磊, 王剑萍, 王华. 抗坏血酸对细菌脂多糖引起发育毒性保护作用[J]. 中国公共卫生, 2007, 23(2): 141-143. DOI: 10.11847/zgggws2007-23-02-08
引用本文: 陈远华, 徐德祥, 赵磊, 王剑萍, 王华. 抗坏血酸对细菌脂多糖引起发育毒性保护作用[J]. 中国公共卫生, 2007, 23(2): 141-143. DOI: 10.11847/zgggws2007-23-02-08
CHEN Yuanhua, XU De-xiang, ZHAO Lei, . Protective effect of ascorbic acid on lipopolysaccharide-induced intra-uterine growth retardation in mice[J]. Chinese Journal of Public Health, 2007, 23(2): 141-143. DOI: 10.11847/zgggws2007-23-02-08
Citation: CHEN Yuanhua, XU De-xiang, ZHAO Lei, . Protective effect of ascorbic acid on lipopolysaccharide-induced intra-uterine growth retardation in mice[J]. Chinese Journal of Public Health, 2007, 23(2): 141-143. DOI: 10.11847/zgggws2007-23-02-08

抗坏血酸对细菌脂多糖引起发育毒性保护作用

Protective effect of ascorbic acid on lipopolysaccharide-induced intra-uterine growth retardation in mice

  • 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15~17 d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AA。所有孕鼠于妊娠第18 d处死。实验2:LPS组小鼠于妊娠第16 d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6 h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+AA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。AA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AA预处理的作用强于后处理。结论 AA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。

     

    Abstract: Objective To investigate the effects of ascorbic acid(AA)on lipopolysaccharide(LPS)-induced intra-uterine fetal death(IUFD),intra-uterine growth retardation(IUGR)and skeletal development retardation in mice.Methods Experiment 1:all pregnant mice except controls(either saline or AA)received an intraperitoneal(75μg/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-induced lipid peroxidation,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-treatmenthad less effect on LPS-induced IUFD.

     

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