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摘要
Introduction: Previous work conducted by our group has shown that nicotine reduces lipopolysaccharide (LPS)-induced systemic inflammatory responses and protects fetuses in pregnant Sprague-Dawley (SD) rats. In the present study, we aim to evaluate the influence of nicotine on rat placenta, including cytokine release, leukocyte infiltration, and alpha 7 nicotinic acetylcholine receptor (alpha 7-nAChR) expression. @@@ Methods: Placental tissues of SD rats on gestation day 14 (GD14) were obtained and cultured in the presence or absence of LPS and/or nicotine. Culture media after 24 h were analyzed for cytokines release using Luminex. Other pregnant SD rats were first pretreated with nicotine on GD14 and GD15, followed by LPS injection on GD16. Placentas were collected on GD18 for H&E staining to evaluate leukocyte density and for real-time PCR and western blotting to identify the alpha 7-nAChR expression in different groups. @@@ Results: Nicotine suppresses LPS-stimulated placental proinflammatory cytokines (IL-1, IL-2, IL-6, TNF-alpha, IFN-gamma) production except IL-17 in vitro, and reduces leucocytes infiltration in the placental chorionic plate caused by LPS in vivo. Moreover, LPS increases the alpha 7-nAChR protein expression in placentas while pretreatment of nicotine inhibits it. @@@ Discussion: These data show that nicotine suppresses LPS-induced placental inflammation by inhibition of cytokine release and infiltration of leukocytes into the placenta, and regulates the increased expression of alpha 7-nAChR in placenta after LPS treatment. Nicotine and other nicotinic agonists may be an alternative therapeutic strategy for placental inflammation.
- 出版日期2016-3
- 单位广州医科大学; 广州市妇女儿童医疗中心
