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N-乙酰半胱氨酸对脂多糖诱发小鼠早产的防治作用
引用本文:蒋学风,曾蔚越,杨开选,徐志红,徐爱群.N-乙酰半胱氨酸对脂多糖诱发小鼠早产的防治作用[J].四川大学学报(医学版),2007,38(2):279-283.
作者姓名:蒋学风  曾蔚越  杨开选  徐志红  徐爱群
作者单位:1. 暨南大学附属第一医院,妇产科,广州,510630
2. 四川大学华西第二医院,妇产科
3. 四川大学华西第二医院,病理科
摘    要:目的 探讨N-乙酰半胱氨酸(NAC)对脂多糖(LPS)诱发小鼠早产的预防和治疗效果及作用机理.方法 将100只孕15 d C57BL/6小鼠随机分为LPS组、NS组、NAC组、治疗作用组和预防作用组,每组20只.在干预后4 h、8 h、12 h、24 h后每个时间点分别处死3只孕鼠,Western Blotting检测子宫组织NF-κB P65,RT-PCR检测IL-8 mRNA水平,试剂盒检测孕鼠血清IL-8、丙二醛(MDA)及超氧化物歧化酶(SOD)浓度,取母、胎肝脏检测谷胱甘肽过氧化物酶(GSH-PX)水平.另每组8只观察NAC对小鼠早产的治疗效果及毒副作用.结果 NAC治疗LPS诱发小鼠早产分娩潜伏期延长至(35.4±2.1) h,活产率为69.0%,NAC预防给药则延长至(44.8±2.6) h,活产率提高至84.3%,与LPS组(15.1±1.9) h,4.3%]相比差异均有统计学意义(P<0.001).LPS作用4 h、8 h、12 h、24 h后,NF-κB活化增强,在4 h达高峰;子宫组织IL-8 mRNA水平、血清IL-8浓度、MDA均升高,在LPS作用8 h后最高;而活胎率、母胎肝脏GSH-PX以及血清SOD水平均下降,在作用8 h最低.预防作用组和治疗作用组各指标变化程度均减弱,同LPS组比较差异均有统计学意义(P<0.05).结论 NAC对LPS诱发的小鼠早产防治效果明显,且预防作用大于治疗作用.

关 键 词:早产  脂多糖  N-乙酰半胱氨酸  白细胞介素8  乙酰半胱氨酸  脂多糖  小鼠  早产分娩  防治作用  Mice  Labor  Preterm  Induced  Lipopolysaccharide  防治效果  比较差异  变化程度  指标  母胎  增强  活化  统计学意义  潜伏期延长  预防给药
收稿时间:2006-05-12
修稿时间:2006-11-08

Effect of N-acetylcysteine on Lipopolysaccharide Induced Preterm Labor in Mice
JIANG Xue-feng,ZENG Wei-yue,YANG Kai-xuan,XU Zhi-hong,XU Ai-qun.Effect of N-acetylcysteine on Lipopolysaccharide Induced Preterm Labor in Mice[J].Journal of West China University of Medical Sciences,2007,38(2):279-283.
Authors:JIANG Xue-feng  ZENG Wei-yue  YANG Kai-xuan  XU Zhi-hong  XU Ai-qun
Institution:Department of Obstetrics and Gynecology, The first Affiliated Hospital, Jinan University, Guangzhou 510630, China.
Abstract:OBJECTIVE: To test the effect of N-acetylcysteine (NAC) on the mice with infection associated preterm labor. METHODS: The pregnant C57BL/6 mice were randomly distributed into five groups, each with 20 mice and were given lipopolysaccharide (LPS), saline solution (NS), NAC, LPS+NAC (therapy), and NAC+ LPS (prevention) respectively. The LPS (20 microg) was injected intraperitoneally to the mice every 12 hours since day 16 of gestation to induce preterm labor. The NAC was orally administered (0.5 g/kg) every 12 hours since day 15 or day 16 for the prevention and therapy groups respectively. The latency interval (from LPS injection to delivery of the first pup) and fetal survival rates were recorded in eight mice from each group. The remaining mice were killed at 4, 8, 12, and 24 hours after the LPS injection (three for a group each time). The NF-kappaB activity and IL-8 mRNA in uterine and maternal and fetal hepatic GSH-PX and serum IL-8, MDA, and SOD were examined. RESULTS: The average latency interval of LPS-treated mice was (15.1 +/- 1.9) hours, with a fetal survival rate of 4.3%. The NAC therapy extended the latency interval of LPS-treated mice to (35.4 +/- 2.1) hours, with a fetal survival rate of 69.0%. The NAC prevention extended the latency interval of LPS-treated mice to (44.8 +/- 2.6) hours, with a fetal survival rate of 84.3%. The expression of NF-KB P65 was activated and reached the peak 4 hours after the LPS injection. The uterine IL-8 mRNA and serum IL-8 and MDA reached the peak whereas the maternal and fetal hepatic GSH and SOD declined to the lowest 8 hours after the LPS injection. The NAC significantly inhibited the effect induced by the LPS (P < 0.01). CONCLUSION: The NAC has a therapeutic effect on the LPS-induced preterm labor in mice. It is even better to be used in preventing preterm labor. The mechanism of the protective effect of NAC may include the deactivation of the NF-kappaB/IL-8 and the reduce of the production of ROS.
Keywords:Preterm labor  Lipopolysaccharide  N-acetylcysteine  IL-8
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