Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation-induced oxidative stress in a mouse model

Ji Yeon Lee, Su Li, Na E. Shin, Quan Na, Jie Dong, Bei Jia, Kimberly Jones-Beatty, Michael W. McLane, Maide Ozen, Jun Lei, Irina Burd

Research output: Contribution to journalArticle

Abstract

Melatonin has been shown to reduce oxidative stress and mitigate hypercoagulability. We hypothesized that maternally administered melatonin may reduce placental oxidative stress and hypercoagulability associated with exposure to intrauterine inflammation (IUI) and consequently improve fetoplacental blood flow and fetal sequelae. Mice were randomized to the following groups: control (C), melatonin (M), lipopolysaccharide (LPS; a model of IUI) (L), and LPS with melatonin (ML). The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. The systolic/diastolic ratio, resistance index, and pulsatility index in uterine artery (UtA) and umbilical artery (UA) were significantly increased in L compared with other groups when analyzed by Doppler ultrasonography. The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. Vascular endothelial damage and thrombi formation, as evidenced by fibrin deposits, were similarly increased in L compared to other groups. Maternal pretreatment with melatonin appears to modulate maternal placental malperfusion, fetal cardiovascular compromise, and fetal neuroinflammation induced by IUI through its antioxidant properties.

Original languageEnglish (US)
Article numbere12591
JournalJournal of pineal research
DOIs
StatePublished - Jan 1 2019

Fingerprint

Melatonin
Oxidative Stress
Inflammation
Thrombophilia
Antioxidants
Placenta
Mothers
Doppler Ultrasonography
Uterine Artery
Umbilical Arteries
Fibrin
Fetal Blood
Blood Vessels
Lipopolysaccharides
Thrombosis
Control Groups

Keywords

  • Doppler ultrasonography
  • intrauterine inflammation
  • melatonin
  • mice
  • placenta
  • placental insufficiency
  • pregnancy

ASJC Scopus subject areas

  • Endocrinology

Cite this

Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation-induced oxidative stress in a mouse model. / Lee, Ji Yeon; Li, Su; Shin, Na E.; Na, Quan; Dong, Jie; Jia, Bei; Jones-Beatty, Kimberly; McLane, Michael W.; Ozen, Maide; Lei, Jun; Burd, Irina.

In: Journal of pineal research, 01.01.2019.

Research output: Contribution to journalArticle

@article{baf3d1908bb64e0885161cd2e4e2d42d,
title = "Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation-induced oxidative stress in a mouse model",
abstract = "Melatonin has been shown to reduce oxidative stress and mitigate hypercoagulability. We hypothesized that maternally administered melatonin may reduce placental oxidative stress and hypercoagulability associated with exposure to intrauterine inflammation (IUI) and consequently improve fetoplacental blood flow and fetal sequelae. Mice were randomized to the following groups: control (C), melatonin (M), lipopolysaccharide (LPS; a model of IUI) (L), and LPS with melatonin (ML). The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. The systolic/diastolic ratio, resistance index, and pulsatility index in uterine artery (UtA) and umbilical artery (UA) were significantly increased in L compared with other groups when analyzed by Doppler ultrasonography. The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. Vascular endothelial damage and thrombi formation, as evidenced by fibrin deposits, were similarly increased in L compared to other groups. Maternal pretreatment with melatonin appears to modulate maternal placental malperfusion, fetal cardiovascular compromise, and fetal neuroinflammation induced by IUI through its antioxidant properties.",
keywords = "Doppler ultrasonography, intrauterine inflammation, melatonin, mice, placenta, placental insufficiency, pregnancy",
author = "Lee, {Ji Yeon} and Su Li and Shin, {Na E.} and Quan Na and Jie Dong and Bei Jia and Kimberly Jones-Beatty and McLane, {Michael W.} and Maide Ozen and Jun Lei and Irina Burd",
year = "2019",
month = "1",
day = "1",
doi = "10.1111/jpi.12591",
language = "English (US)",
journal = "Journal of Pineal Research",
issn = "0742-3098",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation-induced oxidative stress in a mouse model

AU - Lee, Ji Yeon

AU - Li, Su

AU - Shin, Na E.

AU - Na, Quan

AU - Dong, Jie

AU - Jia, Bei

AU - Jones-Beatty, Kimberly

AU - McLane, Michael W.

AU - Ozen, Maide

AU - Lei, Jun

AU - Burd, Irina

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Melatonin has been shown to reduce oxidative stress and mitigate hypercoagulability. We hypothesized that maternally administered melatonin may reduce placental oxidative stress and hypercoagulability associated with exposure to intrauterine inflammation (IUI) and consequently improve fetoplacental blood flow and fetal sequelae. Mice were randomized to the following groups: control (C), melatonin (M), lipopolysaccharide (LPS; a model of IUI) (L), and LPS with melatonin (ML). The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. The systolic/diastolic ratio, resistance index, and pulsatility index in uterine artery (UtA) and umbilical artery (UA) were significantly increased in L compared with other groups when analyzed by Doppler ultrasonography. The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. Vascular endothelial damage and thrombi formation, as evidenced by fibrin deposits, were similarly increased in L compared to other groups. Maternal pretreatment with melatonin appears to modulate maternal placental malperfusion, fetal cardiovascular compromise, and fetal neuroinflammation induced by IUI through its antioxidant properties.

AB - Melatonin has been shown to reduce oxidative stress and mitigate hypercoagulability. We hypothesized that maternally administered melatonin may reduce placental oxidative stress and hypercoagulability associated with exposure to intrauterine inflammation (IUI) and consequently improve fetoplacental blood flow and fetal sequelae. Mice were randomized to the following groups: control (C), melatonin (M), lipopolysaccharide (LPS; a model of IUI) (L), and LPS with melatonin (ML). The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. The systolic/diastolic ratio, resistance index, and pulsatility index in uterine artery (UtA) and umbilical artery (UA) were significantly increased in L compared with other groups when analyzed by Doppler ultrasonography. The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro-inflammatory mediators was significantly increased in L compared to C and ML. Vascular endothelial damage and thrombi formation, as evidenced by fibrin deposits, were similarly increased in L compared to other groups. Maternal pretreatment with melatonin appears to modulate maternal placental malperfusion, fetal cardiovascular compromise, and fetal neuroinflammation induced by IUI through its antioxidant properties.

KW - Doppler ultrasonography

KW - intrauterine inflammation

KW - melatonin

KW - mice

KW - placenta

KW - placental insufficiency

KW - pregnancy

UR - http://www.scopus.com/inward/record.url?scp=85068638077&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85068638077&partnerID=8YFLogxK

U2 - 10.1111/jpi.12591

DO - 10.1111/jpi.12591

M3 - Article

C2 - 31231832

AN - SCOPUS:85068638077

JO - Journal of Pineal Research

JF - Journal of Pineal Research

SN - 0742-3098

M1 - e12591

ER -