Department of Obstetrics and Gynecology,Rambam Health Care Campus, 8 Ha'alya St., 38302, Haifa, Israel.
Department of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine, Lenox Hill Hospital, Northwell Health, New York City, NY, USA.
Reprod Sci. 2021 Jan;28(1):166-176. doi: 10.1007/s43032-020-00272-w. Epub 2020 Aug 24.
Maternal natural vaginal progesterone (nVP) administration has been shown to reduce the risk of preterm birth (PTB). The largest randomized trial of nVP for PTB (OPPTIMUM) noted a sonographic reduction in neonatal brain injury following nVP treatment. We investigated the neuroinflammatory protective effect of maternal nVP in a mouse model for maternal inflammation. Pregnant mice (n = 24) were randomized to nVP (1 mg/day) or vehicle from days 13-16 of gestation. At days 15 and 16, lipopolysaccharide (30 μg) or saline were administered. Mice were sacrificed 4 h following the last injection. Fetal brains and placentas were collected. Levels of NF-κB, nNOS, IL-6, and TNFα were determined by Western blot. Maternal lipopolysaccharide significantly increased fetal brain levels of IL-6 (0.33 ± 0.02 vs. 0.11 ± 0.01 u), TNFα (0.3 ± 0.02 vs. 0.10 ± 0.01 u), NF-κB (0.32 ± 0.01 vs. 0.17 ± 0.01 u), and nNOS (0.24 ± 0.04 vs. 0.08 ± 0.01 u), and reduced the total glutathione levels (0.014 ± 0.001 vs. 0.026 ± 0.001 pmol/μl; p < 0.01) compared with control. Maternal nVP significantly reduced fetal brain levels of IL-6 (0.14 ± 0.01 vs. 0.33 ± 0.02 u), TNFα (0.2 ± 0.06 vs. 0.3 ± 0.02 u), NF-κB (0.16 ± 0.01 vs 0.32 ± 0.01 u), and nNOS (0.14 ± 0.01 vs 0.24 ± 0.04 u), and prevented the reduction of fetal brain total glutathione levels (0.022 ± 0.001 vs. 0.014 ± 0.001 pmol/μl; p < 0.01) to levels similar to controls. A similar pattern was demonstrated in the placenta. Maternal nVP for PTB may protect the fetal brain from inflammation-induced brain injury by inhibiting specific inflammatory and oxidative pathways in both brain and placenta.
母体天然阴道黄体酮(nVP)的给药已被证明可降低早产(PTB)的风险。最大的 nVP 用于 PTB 的随机试验(OPPTIMUM)指出,nVP 治疗后新生儿脑损伤的超声减少。我们在母体炎症的小鼠模型中研究了母体 nVP 的神经炎症保护作用。将怀孕的小鼠(n = 24)随机分为 nVP(1mg/天)或载体,从妊娠第 13-16 天开始。在第 15 和 16 天,给予脂多糖(30μg)或盐水。末次注射后 4 小时处死小鼠。收集胎儿大脑和胎盘。通过 Western blot 测定 NF-κB、nNOS、IL-6 和 TNFα 的水平。母体脂多糖显着增加了胎儿大脑中 IL-6(0.33±0.02 与 0.11±0.01u)、TNFα(0.3±0.02 与 0.10±0.01u)、NF-κB(0.32±0.01 与 0.17±0.01u)和 nNOS(0.24±0.04 与 0.08±0.01u)的水平,并降低了总谷胱甘肽水平(0.014±0.001 与 0.026±0.001pmol/μl;p<0.01)与对照相比。母体 nVP 显着降低了胎儿大脑中 IL-6(0.14±0.01 与 0.33±0.02u)、TNFα(0.2±0.06 与 0.3±0.02u)、NF-κB(0.16±0.01 与 0.32±0.01u)和 nNOS(0.14±0.01 与 0.24±0.04u)的水平,并防止胎儿大脑总谷胱甘肽水平的降低(0.022±0.001 与 0.014±0.001pmol/μl;p<0.01)至与对照相似的水平。在胎盘上也表现出类似的模式。PTB 用母体 nVP 治疗可能通过抑制脑和胎盘内的特定炎症和氧化途径来保护胎儿大脑免受炎症引起的脑损伤。