Department of Medical Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Medical Genetics, School of Medicine, Bam University of Medical Sciences, Bam, Iran.
Biofactors. 2020 May;46(3):341-355. doi: 10.1002/biof.1603. Epub 2019 Dec 24.
Atherosclerosis is a complex and long-lasting disorder characterized by chronic inflammation of arteries that leads to the initiation and progression of lipid-rich plaques, in which monocytes/macrophages play the central role in endothelial inflammation and taking up these lipids. Circulating monocytes can adopt a long-term proinflammatory phenotype leading to their atherogenic activities. During atherogenic condition, inflammatory monocytes adhere to the surface of the activated endothelial cells and then transmigrate across the endothelial monolayer into the intima, where they proliferate and differentiate into macrophages and take up the lipoproteins, forming foam cells that derive atherosclerosis progression. Therefore, modulating the atherogenic activities of inflammatory monocytes can provide a valuable therapeutic approach for atherosclerosis prevention and treatment. Curcumin is a naturally occurring polyphenolic compound with numerous pharmacological activities and shows protective effects against atherosclerosis; however, underlying mechanisms are not clearly known yet. In the present review, on the basis of a growing body of evidence, we show that curcumin can exert antiatherosclerotic effect through inhibiting the atherogenic properties of monocytes, including inflammatory cytokine production, adhesion, and transendothelial migration, as well as intracellular cholesterol accumulation.
动脉粥样硬化是一种复杂且持久的疾病,其特征为动脉的慢性炎症,导致富含脂质的斑块的起始和进展,其中单核细胞/巨噬细胞在血管内皮炎症和摄取这些脂质中起核心作用。循环中的单核细胞可采用长期的促炎表型,导致其动脉粥样硬化活性。在动脉粥样硬化条件下,炎症性单核细胞黏附于活化的内皮细胞表面,然后穿过内皮单层进入内膜,在那里增殖并分化为巨噬细胞并摄取脂蛋白,形成泡沫细胞,导致动脉粥样硬化进展。因此,调节炎症性单核细胞的动脉粥样硬化活性可为动脉粥样硬化的预防和治疗提供有价值的治疗方法。姜黄素是一种天然存在的多酚化合物,具有多种药理学活性,并显示出对动脉粥样硬化的保护作用;然而,其潜在机制尚不清楚。在本综述中,基于越来越多的证据,我们表明姜黄素可以通过抑制单核细胞的动脉粥样硬化特性来发挥抗动脉粥样硬化作用,包括炎症细胞因子的产生、黏附和跨内皮迁移以及细胞内胆固醇的积累。