摘要: 目的 探讨脂多糖对孕鼠胎儿生长的不良影响及烟碱对脂多糖诱导的胎儿生长受限的保护作用。方法 将合笼受孕的妊娠Sprague Dawley大鼠随机分为妊娠对照组、脂多糖组、脂多糖+烟碱组、烟碱对照组：脂多糖组在妊娠第16日腹腔注射脂多糖；脂多糖+烟碱组在妊娠第14日、15日皮下注射烟碱，在妊娠第16日腹腔注射脂多糖；烟碱对照组仅在妊娠第14日、15日皮下注射烟碱；妊娠对照组于妊娠第14日、15日皮下注射生理盐水，妊娠第16日腹腔注射生理盐水。所有孕鼠于妊娠第18日麻醉处死，记录胎儿吸收率、活胎数量及重量、胎盘重量，并收集孕鼠胎盘组织评估其病理学改变，研究脂多糖和烟碱对胎盘病理的影响及对孕鼠胎儿生长的影响。结果 与正常妊娠对照组相比，脂多糖组胚胎吸收率增加、成活胎儿数减少、胎儿体质量及胎盘质量均下降(P＜0.008或0.01)；与脂多糖组相比，脂多糖+烟碱组成活胎儿数、胎儿体质量均增加(P＜0.008或0.01)。胎盘病理显示，脂多糖组孕鼠胎盘出现了明显的病理改变，包括炎性细胞在发育不良绒毛间浸润、绒毛间隙减少及绒毛血管减少，炎性细胞在蜕膜浸润，胎膜炎性坏死；在正常妊娠对照组、烟碱对照组和脂多糖+烟碱组均未发现胎盘组织结构的损伤及大量炎性细胞的浸润。结论 烟碱可减少脂多糖对胎盘组织的损伤，对脂多糖诱导的孕鼠胎儿生长受限起保护作用。

Abstract: Objective To investigate the negative impact of lipopolysaccharide (LPS) upon the fetal growth and evaluate the protective effect of nicotine on the LPS-induced fetal growth restriction (FGR) in pregnant rats. Methods Pregnant Sprague Dawley rats were randomly divided into the control, LPS, LPS + nicotine and nicotine groups. In the LPS group, the rats were intraperitoneally injected with LPS on the 16^th day of gestation. In the LPS + nicotine group, the rats were first pretreated with nicotine by subcutaneous injection on the 14^th and 15^th days of gestation, followed by intraperitoneal injection of LPS on the 16^th day of gestation. In the nicotine group, the rats were subcutaneously injected with nicotine alone on the 14^th and 15^th days of gestation. In the control group, the rats were subcutaneously injected with normal saline on the 14^th and 15^th days of gestation, followed by intraperitoneal injection of normal saline on the 16^th day of gestation. All pregnant rats were sacrificed on the 18th day of gestation. The fetal absorption rate, number and weight of live fetuses, and placental weight were recorded. The placental tissues of pregnant rats were collected to assess the pathological changes and the effect of LPS and nicotine on the pathology of the placenta and on the fetal growth of the pregnant rates was evaluated. Results Compared with the control group, the fetal absorption rate was significantly increased, the number of live fetuses was considerably decreased, and the fetal weight and placental weight were significantly decreased in the LPS group (P < 0.008 or 0.01). Compared with the LPS group, the number of live fetuses and fetal weight were significantly increased in the LPS + nicotine group (P < 0.008 or 0.01). In the LPS group, pathological examination demonstrated obvious pathological changes in the placenta of pregnant rats, including inflammatory cells infiltrating into the poorly-developed villi, reduction of the villi space, and decrease of chorionic vessels, inflammatory cells infiltrating into the decidua, and inflammatory necrosis of fetal membrane. In the control, nicotine and LPS + nicotine groups, neither placental tissue damage nor inflammatory cell infiltration were observed. Conclusion Nicotine can mitigate the LPS-induced placental tissue injury and exert a protective effect upon the LPS-induced FGR in pregnant rates.