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Medical Gas Research

, 2:4

First Online: 20 February 2012Received: 27 September 2011Accepted: 20 February 2012


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 ppmas 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.

Electronic supplementary materialThe online version of this article doi:10.1186-2045-9912-2-4 contains supplementary material, which is available to authorized users.

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Autor: Tarek El-Mousleh - Pablo A Casalis - Ivonne Wollenberg - Maria L Zenclussen - Hans D Volk - Stefanie Langwisch - Federico

Fuente: https://link.springer.com/

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