Melatonin prevents experimental preterm labor and increases offspring survival.

DOMINGUEZ RUBIO AP; SORDELLI MS; SALAZAR A; AISEMBERG J; BARIANI MV; CELLA M; ROSESTEIN RE; FRANCHI AM

JOURNAL OF PINEAL RESEARCH

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2014 p. 154 - 162

0742-3098

Preterm delivery is the leading cause of neonatal mortality and contributes to delayed physical and cognitivedevelopment in children. At present, there is no efficient therapy to prevent preterm labor. A large body of evidencesuggests that intra-amniotic infections may be a significant and potentially preventable cause of preterm birth. Thiswork assessed the effect of melatonin in a murine model of inflammation-associated preterm delivery which mimicscentral features of preterm infection in humans. For this purpose, preterm labor was induced in BALB/c mice byintraperitoneal injections of bacterial lipopolysaccharide (LPS) at 10.00 h (10 =g LPS) and 13.00 h (20 =g LPS) onday 15 of pregnancy. On day 14 of pregnancy, a pellet of melatonin (25 mg) had been subcutaneously implantedinto a group of animals. In the absence of melatonin, a 100% incidence of preterm birth was observed in LPS-treatedanimals, and the fetuses showed widespread damage. By comparison, treatment with melatonin prevented pretermbirth in 50% of the cases, and all pups from melatonin-treated females were born alive and their body weight did notdiffer from control animals. Melatonin significantly prevented the LPS-induced rises in uterine prostaglandin (PG)E2, PGF2α, and cyclooxygenase-2 protein levels. In addition, melatonin prevented the LPS-induced increase inuterine nitric oxide (NO) production, inducible NO synthase protein and tumor necrosis factor-alpha (TNFα) levels.Collectively, our results suggest that melatonin could be a new therapeutic tool to prevent preterm labor and toincrease offspring survival.