Artículos de revistas
Melatonin prevents experimental preterm labor and increases offspring survival
Fecha
2014-03Registro en:
Domínguez Rubio, Ana Paula; Sordelli, Micaela Soledad; Salazar, Ana Inés; Aisemberg, Julieta; Bariani, Maria Victoria; et al.; Melatonin prevents experimental preterm labor and increases offspring survival; John Wiley & Sons Ltd; Journal Of Pineal Research; 56; 2; 3-2014; 154-162
0742-3098
Autor
Domínguez Rubio, Ana Paula
Sordelli, Micaela Soledad
Salazar, Ana Inés
Aisemberg, Julieta
Bariani, Maria Victoria
Cella, Maximiliano
Rosenstein, Ruth Estela
Franchi, Ana Maria
Resumen
Preterm delivery is the leading cause of neonatal mortality and contributes to delayed physical and cognitive development in children. At present, there is no efficient therapy to prevent preterm labor. A large body of evidence suggests that intra-amniotic infections may be a significant and potentially preventable cause of preterm birth. This work assessed the effect of melatonin in a murine model of inflammation-associated preterm delivery which mimics central features of preterm infection in humans. For this purpose, preterm labor was induced in BALB/c mice by intraperitoneal injections of bacterial lipopolysaccharide (LPS) at 10.00 hr (10 μg LPS) and 13.00 hr (20 μg LPS) on day 15 of pregnancy. On day 14 of pregnancy, a pellet of melatonin (25 mg) had been subcutaneously implanted into a group of animals. In the absence of melatonin, a 100% incidence of preterm birth was observed in LPS-treated animals, and the fetuses showed widespread damage. By comparison, treatment with melatonin prevented preterm birth in 50% of the cases, and all pups from melatonin-treated females were born alive and their body weight did not differ 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 in uterine 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 to increase offspring survival.