Mental stress promotes the proliferation of endometriotic lesions in mice.


Journal

Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353

Informations de publication

Date de publication:
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

155222

Informations 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.

Auteurs

Takako Kawakita (T)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan. Electronic address: kawakita.takako@tokushima-u.ac.jp.

Takeshi Kato (T)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

Takeshi Iwasa (T)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

Otgontsetseg Erdenebayar (O)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

Yuri Kadota (Y)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

Kana Kasai (K)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

Kanako Yoshida (K)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

Minoru Irahara (M)

Department of Obstetrics and Gynecology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto cho, Tokushima, Japan.

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Classifications MeSH