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Exploring the potential of low doses carbon monoxide as therapy in pregnancy complications

机译：探索低剂量一氧化碳作为妊娠并发症治疗的潜力

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摘要

Heme Oxygenase-1 (HO-1) has been shown to play a pivotal role in pregnancy outcome and its ablation leads to abnormal placentation, intrauterine fetal growth restriction (IUGR) and subsequent intrauterine fetal death. Carbon monoxide (CO) has been found to mimic the protective effects of HO-1 activity, rescuing HO-1-deficient fetuses. This gasotransmitter arises in biological systems during the oxidative catabolism of heme by HO. Here, we explored the potential of CO in preventing IUGR and established the optimal doses and therapeutic time window in a clinically relevant mouse model. We additionally investigated the pathways activated upon CO application in vivo. We established 50 ppm as the best lowest dose of CO necessary to prevent growth restriction being the optimal time frame during days 3 to 8 of mouse pregnancy. CO lead to higher fetal and placental weights and avoided fetal death without showing any pathologic effects. CO breathing further suppressed inflammatory responses, diminished placenta apoptosis and complement deposition and regulated placental angiogenesis. Our results confirm the protective role of the HO-1/CO axis and point this gas as an emerging therapeutic possibility which is worth to further explore.
机译：血红素加氧酶-1（HO-1）已显示在妊娠结局中起关键作用，其消融可导致异常胎盘，宫内胎儿生长受限（IUGR）和随后的宫内胎儿死亡。已经发现一氧化碳（CO）可以模仿HO-1活性的保护作用，拯救缺乏HO-1的胎儿。这种气体递质在HO氧化血红素的氧化分解代谢过程中出现在生物系统中。在这里，我们探索了CO预防IUGR的潜力，并在临床相关的小鼠模型中建立了最佳剂量和治疗时间窗。我们还研究了在体内应用CO激活的途径。我们确定50 ppm作为防止生长受限所需的最佳CO最低剂量是小鼠妊娠第3至8天的最佳时间范围。一氧化碳导致胎儿和胎盘重量增加，避免了胎儿死亡，而没有任何病理影响。一氧化碳呼吸可进一步抑制炎症反应，减少胎盘凋亡和补体沉积并调节胎盘血管生成。我们的结果证实了HO-1 / CO轴的保护作用，并指出这种气体是一种新兴的治疗可能性，值得进一步探讨。

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