Skip to main content
padlock icon - secure page this page is secure

Melatonin alleviates lipopolysaccharide-induced placental cellular stress response in mice

Buy Article:

$52.00 + tax (Refund Policy)

Abstract: 

Melatonin protects mice from lipopolysaccharide (LPS)-induced fetal death and intra-uterine growth retardation. Nevertheless, its molecular mechanism remains obscure. In the present study, we investigated the effects of melatonin on LPS-induced cellular stress in placenta. Pregnant mice were given with melatonin [5.0 mg/kg, intraperitoneal (i.p.)] 30 min before and 150 min after LPS (300 μg/kg, i.p.) on gestational day 15. Oxidative stress, endoplasmic reticulum (ER) stress, hypoxic stress, and heat stress in placenta were analyzed at 4 hr after LPS. As expected, maternal LPS administration resulted in placental glutathione (GSH) depletion and up-regulated the expression of placental antioxidative enzymes. In addition, LPS significantly increased the level of inducible nitric oxide synthase (iNOS) and enhanced the intensity of placental 3-nitrotyrosine residues. An ER stress, as determined by a decreased GRP78 expression, an obvious eIF2α and JNK phosphorylation, and an increased CHOP expression, were observed in placenta of pregnant mice injected with LPS. In addition, LPS significantly increased mRNA level of placental HIF-1α, VEGF, and ET-1, the markers of hypoxic stress. Heme oxygenase (HO)-1, a marker of heat stress, was also up-regulated in placenta of LPS-treated pregnant mice. Interestingly, LPS-induced placental oxidative stress, hypoxic stress, and ER stress were significantly alleviated when pregnant mice were given with melatonin, whereas melatonin had little effect on LPS-evoked placental HO-1 expression. In conclusion, maternally administered melatonin alleviates LPS-induced cellular stress in the placenta. Melatonin may be useful as pharmacological agents to protect the fetuses against LPS-induced intra-uterine fetal death and intra-uterine growth restriction.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: endoplasmic reticulum stress; heat stress; hypoxic stress; lipopolysaccharide; melatonin; oxidative stress; placenta

Document Type: Research Article

Publication date: May 1, 2011

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more