Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice

Standard

Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. / Steffens, Sabine; Veillard, Niels R; Arnaud, Claire; Pelli, Graziano; Burger, Fabienne; Staub, Christian; Karsak, Meliha; Zimmer, Andreas; Frossard, Jean-Louis; Mach, François.

in: NATURE, Jahrgang 434, Nr. 7034, 07.04.2005, S. 782-6.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Steffens, S, Veillard, NR, Arnaud, C, Pelli, G, Burger, F, Staub, C, Karsak, M, Zimmer, A, Frossard, J-L & Mach, F 2005, 'Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice', NATURE, Jg. 434, Nr. 7034, S. 782-6. https://doi.org/10.1038/nature03389

APA

Steffens, S., Veillard, N. R., Arnaud, C., Pelli, G., Burger, F., Staub, C., Karsak, M., Zimmer, A., Frossard, J-L., & Mach, F. (2005). Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. NATURE, 434(7034), 782-6. https://doi.org/10.1038/nature03389

Vancouver

Steffens S, Veillard NR, Arnaud C, Pelli G, Burger F, Staub C et al. Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. NATURE. 2005 Apr 7;434(7034):782-6. https://doi.org/10.1038/nature03389

Bibtex

@article{133e639fb2f0407cbc78659b7194b77c,
title = "Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice",
abstract = "Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.",
keywords = "Animals, Apolipoproteins E/deficiency, Arteriosclerosis/complications, Cells, Cultured, Chemotaxis, Leukocyte/drug effects, Disease Models, Animal, Disease Progression, Dronabinol/administration & dosage, Humans, Inflammation/complications, Interferon-gamma/metabolism, Macrophages/cytology, Mice, Mice, Knockout, RNA, Messenger/genetics, Receptor, Cannabinoid, CB2/antagonists & inhibitors, Receptors, CCR2, Receptors, Chemokine/genetics, Survival Rate, Th1 Cells/cytology, Thioglycolates/pharmacology, Tumor Necrosis Factor-alpha/pharmacology",
author = "Sabine Steffens and Veillard, {Niels R} and Claire Arnaud and Graziano Pelli and Fabienne Burger and Christian Staub and Meliha Karsak and Andreas Zimmer and Jean-Louis Frossard and Fran{\c c}ois Mach",
year = "2005",
month = apr,
day = "7",
doi = "10.1038/nature03389",
language = "English",
volume = "434",
pages = "782--6",
journal = "NATURE",
issn = "0028-0836",
publisher = "NATURE PUBLISHING GROUP",
number = "7034",

}

RIS

TY - JOUR

T1 - Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice

AU - Steffens, Sabine

AU - Veillard, Niels R

AU - Arnaud, Claire

AU - Pelli, Graziano

AU - Burger, Fabienne

AU - Staub, Christian

AU - Karsak, Meliha

AU - Zimmer, Andreas

AU - Frossard, Jean-Louis

AU - Mach, François

PY - 2005/4/7

Y1 - 2005/4/7

N2 - Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.

AB - Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.

KW - Animals

KW - Apolipoproteins E/deficiency

KW - Arteriosclerosis/complications

KW - Cells, Cultured

KW - Chemotaxis, Leukocyte/drug effects

KW - Disease Models, Animal

KW - Disease Progression

KW - Dronabinol/administration & dosage

KW - Humans

KW - Inflammation/complications

KW - Interferon-gamma/metabolism

KW - Macrophages/cytology

KW - Mice

KW - Mice, Knockout

KW - RNA, Messenger/genetics

KW - Receptor, Cannabinoid, CB2/antagonists & inhibitors

KW - Receptors, CCR2

KW - Receptors, Chemokine/genetics

KW - Survival Rate

KW - Th1 Cells/cytology

KW - Thioglycolates/pharmacology

KW - Tumor Necrosis Factor-alpha/pharmacology

U2 - 10.1038/nature03389

DO - 10.1038/nature03389

M3 - SCORING: Journal article

C2 - 15815632

VL - 434

SP - 782

EP - 786

JO - NATURE

JF - NATURE

SN - 0028-0836

IS - 7034

ER -