Mental stress promotes the proliferation of endometriotic lesions in mice.
Adipose Tissue
/ metabolism
Animals
Cell Proliferation
/ physiology
Chemokine CCL2
/ metabolism
Cytokines
/ metabolism
Disease Models, Animal
Endometriosis
/ metabolism
Endometrium
/ metabolism
Female
Inflammation
/ metabolism
Inflammation Mediators
/ metabolism
Mice
Mice, Inbred C57BL
Signal Transduction
/ physiology
Stress, Psychological
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Adipose
Cytokine
Endometriosis
Inflammation
Mice
Stress
Journal
Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
07
12
2019
revised:
02
07
2020
accepted:
23
07
2020
pubmed:
10
8
2020
medline:
15
12
2021
entrez:
10
8
2020
Statut:
ppublish
Résumé
Endometriosis is a condition in which tissue similar to the womb lining begins to grow in other sites, such as the ovaries or fallopian tubes. Endometriosis can cause pelvic pain, adhesion formation, and infertility. Here, we investigated the relationship between deterioration of endometriosis and inflammation of intraperitoneal adipose tissue in mice. We created a mouse model of endometriosis, then subjected these mice to stress loading. In the experimental mice, we measured protein expression levels of prostaglandin-E2, monocyte chemoattractant protein-1, and tumor necrosis factor-α using ELISA kits. We used quantitative real-time polymerase chain reaction to measure mRNA expression levels of inflammation-related enzymes and cytokines in lesions and adipose tissues. This study sugest that endometriotic lesions may progress in the presence of psychological stress in the presence of endometriosis. In addition, inflammation of the adipose tissue around the uterus may be involved in the development of endometriosis. However, this needs further consideration. Reducing or avoiding stress as much as possible may prevent the progression of endometriosis.
Identifiants
pubmed: 32768923
pii: S1043-4666(20)30238-6
doi: 10.1016/j.cyto.2020.155222
pii:
doi:
Substances chimiques
Chemokine CCL2
0
Cytokines
0
Inflammation Mediators
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
155222Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.