Mangiferin ameliorates gestational diabetes mellitus-induced placental oxidative stress, inflammation and endoplasmic reticulum stress and improves fetal outcomes in mice.
Animals
Atherosclerosis
/ drug therapy
Diabetes, Gestational
/ drug therapy
Endoplasmic Reticulum Stress
/ drug effects
Female
Fetus
/ diagnostic imaging
Inflammation
/ drug therapy
Insulin Resistance
Lipid Metabolism
/ drug effects
Mice
Mice, Inbred C57BL
Oxidative Stress
/ drug effects
Placenta
/ drug effects
Pregnancy
Xanthones
/ pharmacology
Endoplasmic reticulum stress
Gestational diabetes mellitus
Inflammation
Mangiferin
Oxidative stress
Journal
European journal of pharmacology
ISSN: 1879-0712
Titre abrégé: Eur J Pharmacol
Pays: Netherlands
ID NLM: 1254354
Informations de publication
Date de publication:
15 Sep 2019
15 Sep 2019
Historique:
received:
01
06
2019
revised:
18
06
2019
accepted:
01
07
2019
pubmed:
6
7
2019
medline:
29
1
2020
entrez:
6
7
2019
Statut:
ppublish
Résumé
Gestational diabetes mellitus (GDM) is a temporary form of diabetes during pregnancy, which causes maternal diabetic symptoms and abnormal fetal development, and influence the health of maternal-child in clinical practice. Mangiferin is a bioactive ingredient with anti-inflammation, anti-oxidation and anti-endoplasmic reticulum stress activities. In current study, the effects of mangiferin on GDM were evaluated. We reported that mangiferin greatly improved altered glucose and lipid profile, insulin tolerance, and reproductive outcomes of the GDM mice. Mangiferin ameliorated placental oxidative stress, inflammation and ER stress in GDM mice. Therefore, we demonstrated that mangiferin displayed protective effects on gestational diabetes mellitus symptoms by suppressing placental oxidative stress, inflammation and endoplasmic reticulum stress in GDM mice.
Identifiants
pubmed: 31276667
pii: S0014-2999(19)30474-1
doi: 10.1016/j.ejphar.2019.172522
pii:
doi:
Substances chimiques
Xanthones
0
mangiferin
1M84LD0UMD
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
172522Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.