Abstract |
Genital tract infections caused by Gram-negative bacteria induce miscarriage and are one of the most common complications of human pregnancy. LPS administration to 7-day pregnant mice induces embryo resorption after 24h, with nitric oxide playing a fundamental role in this process. We have previously shown that progesterone exerts protective effects on the embryo by modulating the inflammatory reaction triggered by LPS. Here we sought to investigate whether the in vivo administration of progesterone modulated the LPS-induced nitric oxide production from peripheral blood mononuclear cells from pregnant and non-pregnant mice. We found that progesterone downregulated LPS-induced nitric oxide production by a progesterone receptor-independent mechanism. Moreover, our results suggest a possible participation of glucocorticoid receptors in at least some of the anti-inflammatory effects of progesterone.
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Authors | Manuel Luis Wolfson, Julieta Aylen Schander, María Victoria Bariani, Fernando Correa, Ana María Franchi |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 769
Pg. 110-6
(Dec 15 2015)
ISSN: 1879-0712 [Electronic] Netherlands |
PMID | 26548622
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2015 Elsevier B.V. All rights reserved. |
Chemical References |
- Lipopolysaccharides
- Receptors, Glucocorticoid
- Receptors, Progesterone
- Nitric Oxide
- Progesterone
- Nitric Oxide Synthase
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Topics |
- Animals
- BALB 3T3 Cells
- Embryo Loss
(chemically induced, prevention & control)
- Female
- Leukocytes, Mononuclear
(drug effects, metabolism)
- Lipopolysaccharides
(pharmacology)
- Mice
- Nitric Oxide
(biosynthesis)
- Nitric Oxide Synthase
(metabolism)
- Pregnancy
- Progesterone
(pharmacology)
- Receptors, Glucocorticoid
(metabolism)
- Receptors, Progesterone
(metabolism)
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