The molecular analysis of placental abruption using in vitro placental model

宫内感染是胎盘早剥的关键触发因素。为了分析炎性细胞因子在胎盘病变中的作用，我们检测了重度绒毛膜羊膜炎(CAM)胎盘中多种细胞因子的表达模式，发现IL-6主要表达于绒毛间质中的巨噬细胞。利用实验性脂多糖(LPS)诱导的PTD模型，研究了靶向该细胞因子的治疗潜力。在内毒素治疗前注射抗IL-6受体抗体(MR16-1)。MR16-1组小鼠的PTD发生率(17%)明显低于对照组的53%。结果，MR16-1治疗显著延长了妊娠期，对小鼠及其幼崽没有任何明显的不良反应。因此，靶向IL-6信号转导可能是预防胎盘早剥的一种有前景的选择，并需要进一步探索以用于未来的临床应用。

Intrauterine infection is a key trigger of placental abruption. In order to analyze the potential role of inflammatory cytokines in this pathogenesis, we examined the expressional pattern of various cytokines in placentae complicated with severe chorioamnionitis (CAM) and found that IL-6 is mainly expressed in macrophages in villous mesenchyme. Using an experimental lipopolysaccharide (LPS)-induced PTD model, the therapeutic potential of targeting this cytokine was investigated. Anti-IL-6 receptor antibody (MR16-1) was delivered before LPS treatment. Mice in the MR16-1 group had a significantly lower rate of PTD (17%) than 53% in the controls. As a result, MR16-1 treatment significantly prolonged the gestational period without any apparent adverse events on the mice and their pups. Thus, targeting IL-6 signaling can be a promising option for the prevention of placental abruption and needs to be further explored for future clinical application.