CD36 is a scavenger receptor known to play a critical role in the development of atherosclerosis by mediating the uptake of oxidized low-density lipoproteins (oxLDL) by macrophages. thus leading to foam cell formation. It is now generally recognized that the immune system has a pivotal role in the pathogenesis of atherosclerosis, whose progression is determined by ongoing inflammatory reactions. Recently, several studies pointed out that opioid peptides exert anti-inflammatory activities. Therefore the aim of the present study was to evaluate a possible endomorphin-1 (EM-1) immunomodulatory activity on human foam cells. Our results showed that EM-1 reduced Nile Red-stained lipid droplets content, decreased the expression of CD36 receptor and modulated tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) release from lipid-laden macrophages. Furthermore, Naloxone, an opioid receptors antagonist, reverted the anti-atherogenic and anti-inflammatory observed effects of EM-1. These data demonstrated, for the first time, an unprecedented ability of EM-1 to act as a novel modulator for macrophage-to-foam cell transformation, and for inflammatory cytokines profile, suggesting possible novel endomorphin-based anti-atherosclerotic approaches for the prevention and treatment of atherosclerosis. (C) 2010 Elsevier Inc. All rights reserved.

Endomorphin-1 prevents lipid accumulation via CD36 down-regulation and modulates cytokines release from human lipid-laden macrophages

Maccarrone M
2011-01-01

Abstract

CD36 is a scavenger receptor known to play a critical role in the development of atherosclerosis by mediating the uptake of oxidized low-density lipoproteins (oxLDL) by macrophages. thus leading to foam cell formation. It is now generally recognized that the immune system has a pivotal role in the pathogenesis of atherosclerosis, whose progression is determined by ongoing inflammatory reactions. Recently, several studies pointed out that opioid peptides exert anti-inflammatory activities. Therefore the aim of the present study was to evaluate a possible endomorphin-1 (EM-1) immunomodulatory activity on human foam cells. Our results showed that EM-1 reduced Nile Red-stained lipid droplets content, decreased the expression of CD36 receptor and modulated tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) release from lipid-laden macrophages. Furthermore, Naloxone, an opioid receptors antagonist, reverted the anti-atherogenic and anti-inflammatory observed effects of EM-1. These data demonstrated, for the first time, an unprecedented ability of EM-1 to act as a novel modulator for macrophage-to-foam cell transformation, and for inflammatory cytokines profile, suggesting possible novel endomorphin-based anti-atherosclerotic approaches for the prevention and treatment of atherosclerosis. (C) 2010 Elsevier Inc. All rights reserved.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/155662
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 11
  • ???jsp.display-item.citation.isi??? 10
social impact