Antisclerothic effect of tibolone by reducing proinflammatory cytokines expression, ROS production and LDL-ox uptake in THP-1 macrophages.


Journal

Steroids
ISSN: 1878-5867
Titre abrégé: Steroids
Pays: United States
ID NLM: 0404536

Informations de publication

Date de publication:
03 2021
Historique:
received: 13 09 2020
revised: 07 12 2020
accepted: 18 12 2020
pubmed: 1 1 2021
medline: 25 11 2021
entrez: 31 12 2020
Statut: ppublish

Résumé

Cardiovascular disease is more frequent in menopausal women, which has been related to factor such as weight gain, altered fat distribution, and increased inflammation markers including adipokines (MCP-1, TNF-α, IL-6) and cytokines (IL-1, IL-6, TNF-α) produced by macrophages. In addition to their phagocytic activity, macrophages secrete cytokines and chemokines that induces cell recruitment, which is a process related to vascular damage that favors the formation of atheromatous plaques. Tibolone (Tb) therapy is used to reduce the symptoms of menopause as well as osteoporosis and it has been shown to decreases the risk of fractures. To investigate the effect of tibolone in macrophage enzymatic activity, gene expression of cytokines, and its effect on foam cells formation. We use phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells. The cells were incubated 24 h and 48 h using pre and post-treatment schemes. We evaluated total ROS determination by NBT assay, expression of cytokines (IL-1β, IL-6, TNF-α, NOS2, ARG1, TGFβ) by RT-qPCR and foam cell formation in THP-1 differentiated macrophages stimulated with PMA. It was observed that the minor levels of total ROS determination were obtained with tibolone at 48 h in post-treatment scheme. Also, in a long term we found decrease the proinflammatory cytokines (IL-1β, IL-6 and TNF-α). Finally, with treatment for 24 h with P4 y Tb we observed fewer LDL vesicles into macrophages cytoplasm. These results suggest that tibolone reduces the inflammatory process, also inhibits the foam cells formation; suggesting a possible role in reducing cardiovascular risk.

Sections du résumé

BACKGROUND
Cardiovascular disease is more frequent in menopausal women, which has been related to factor such as weight gain, altered fat distribution, and increased inflammation markers including adipokines (MCP-1, TNF-α, IL-6) and cytokines (IL-1, IL-6, TNF-α) produced by macrophages. In addition to their phagocytic activity, macrophages secrete cytokines and chemokines that induces cell recruitment, which is a process related to vascular damage that favors the formation of atheromatous plaques. Tibolone (Tb) therapy is used to reduce the symptoms of menopause as well as osteoporosis and it has been shown to decreases the risk of fractures.
METHODS
To investigate the effect of tibolone in macrophage enzymatic activity, gene expression of cytokines, and its effect on foam cells formation. We use phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells. The cells were incubated 24 h and 48 h using pre and post-treatment schemes. We evaluated total ROS determination by NBT assay, expression of cytokines (IL-1β, IL-6, TNF-α, NOS2, ARG1, TGFβ) by RT-qPCR and foam cell formation in THP-1 differentiated macrophages stimulated with PMA.
RESULTS
It was observed that the minor levels of total ROS determination were obtained with tibolone at 48 h in post-treatment scheme. Also, in a long term we found decrease the proinflammatory cytokines (IL-1β, IL-6 and TNF-α). Finally, with treatment for 24 h with P4 y Tb we observed fewer LDL vesicles into macrophages cytoplasm.
CONCLUSIONS
These results suggest that tibolone reduces the inflammatory process, also inhibits the foam cells formation; suggesting a possible role in reducing cardiovascular risk.

Identifiants

pubmed: 33383063
pii: S0039-128X(20)30205-1
doi: 10.1016/j.steroids.2020.108779
pii:
doi:

Substances chimiques

Cytokines 0
Lipoproteins, LDL 0
Reactive Oxygen Species 0
oxidized low density lipoprotein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

108779

Informations de copyright

Copyright © 2020. Published by Elsevier Inc.

Auteurs

Karla A Aguayo-Cerón (KA)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico.

Gisela Gutiérrez-Iglesias (G)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico.

Alberto Parra-Barrera (A)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico.

María E Ocharan-Hernández (ME)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico.

Rodrigo Romero-Nava (R)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico; Hospital Infantil de México Federico Gómez, Laboratorio de Investigación en Farmacología, Ciudad de México, Mexico.

Carlos A Jiménez-Zamarripa (CA)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico; Hospital Psiquiátrico "Dr. Samuel Ramírez Moreno", Secretaria de Salud, Ciudad de México, Mexico.

Claudia C Calzada-Mendoza (CC)

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional-Escuela Superior de Medicina, Ciudad de México, Mexico. Electronic address: cccalzadam@yahoo.com.mx.

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Classifications MeSH