Thus, Ој-opioid receptor antagonists may be useful for the prevention and treatment of atherosclerosis. Our study provides the first evidence that ОІ-endorphin contributes to the acceleration of the progression and instability of atheromatous plaques. Chronic ОІ-endorphin infusion into Apoe в€’/в€’ mice significantly aggravated the development of aortic atherosclerotic lesions, with an increase in vascular inflammation and the intraplaque macrophage/smooth muscle cell ratio, an index of plaque instability. ОІ-Endorphin also significantly shifted the macrophage phenotype to proinflammatory M1 rather than anti-inflammatory M2 via NF- ОєB phosphorylation during monocyte-macrophage differentiation and increased migration and apoptosis in association with c-jun-N-terminal kinase, p38, and NF- ОєB phosphorylation in HASMCs. ОІ-Endorphin significantly increased HUVEC proliferation and enhanced oxidized low-density lipoprotein-induced foam cell formation in macrophages. ОІ-Endorphin significantly increased THP-1 monocyte adhesion to HUVECs and induced upregulation of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin via nuclear factor- ОєB (NF- ОєB) and p38 phosphorylation in HUVECs. The Ој-opioid receptor (OPRM1) was expressed in THP-1 monocytes, macrophages, HASMCs, HUVECs, and human aortic endothelial cells. We also assessed the effects of ОІ-endorphin on aortic lesions in Apoe в€’/в€’ mice in vivo. We assessed the effects of ОІ-endorphin on the inflammatory response and monocyte adhesion in human umbilical vein endothelial cells (HUVECs), foam cell formation, and the inflammatory phenotype in THP-1 monocyte-derived macrophages, and migration and proliferation of human aortic smooth muscle cells (HASMCs) in vitro.

We clarified the effects of ОІ-endorphin on atherosclerosis.

ОІ-Endorphin induces endothelial dysfunction and is related to insulin resistance.

О’-Endorphin, an endogenous opioid peptide, and its Ој-opioid receptor are expressed in brain, liver, and peripheral tissues.

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