Research paperRole of inflammatory responses in initiation of atherosclerosis: effects of anti-inflammatory drugs on cuff-induced leukocyte accumulation and intimal thickening of rabbit carotid artery
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Glucocorticoids are active players and therapeutic targets in atherosclerotic cardiovascular disease
2020, Molecular and Cellular EndocrinologyCitation Excerpt :The decrease in atherosclerosis burden in dexamethasone-treated rabbits in the study by Asai et al. (1993) coincided with a reduction in the lesional macrophage and lymphocyte content. Notably, findings from Hagihara et al. (1991) have shown that dexamethasone treatment markedly lowers the adhesion of leukocytes to the aortic endothelium, which also explains the dexamethasone-induced protection to cuff-induced intimal thickening observed in Japanese white rabbits. Anti-inflammatory glucocorticoid administration to rabbits, i.e. oral prednisone treatment, similarly reduces the restenosis extent in response to stent implantation into atherosclerosis-containing iliac arteries (Ribichini et al., 2007).
Engineered nanoparticles for the detection, treatment and prevention of atherosclerosis: how close are we?
2017, Drug Discovery TodayCitation Excerpt :Statins have been touted as the gold standard of blood-cholesterol-reducing drugs, lowering LDL levels and atherosclerotic risk [17]. Concurrently, different corticosteroids such as dexamethasone [18] and prednisolone [19] have been widely explored for reducing inflammation. At the later stages of atherosclerosis, anticoagulant or thrombolytic therapies and surgical intervention such as angioplasty, bypass grafting and stenting are more prevalent.
Adipogenic differentiating agents regulate expression of fatty acid binding protein and CD36 in the J744 macrophage cell line
2003, Journal of Lipid ResearchCitation Excerpt :Atherosclerosis-prone mice (apoE−/−) that lack CD36 expression (CD36−/−) have markedly reduced atherosclerotic lesion size (17). Dexamethasone has been shown to decrease atherosclerotic lesion size in several animal models (46–49). However, the role of aP2 and CD36 in the response of atherosclerotic lesion inhibition by dexamethasone remains to be tested.
Pathogenetic heterogeneity of in-stent lesion formation in human peripheral arterial disease
2002, Journal of Vascular SurgeryCitation Excerpt :Although we are now unsure which factor(s) promoted the accumulation of proteoglycans in the inner intima, there is a possibility that an unknown factor is secreted at the luminal surface. An experimental study with an arterial cuff model showed that a cuff, placed around the arterial adventitia, induced adhesion of leukocytes to the luminal surface as an inflammatory response to the foreign body.25,26 Because a stent is also a foreign body, we think that leukocytes in the blood vessel possibly adhere to the surface of the intimal lesion, even though the stent is completely covered by neointima.
Dexamethasone impairs cholesterol egress from a localized lipoprotein depot in vivo
1998, Atherosclerosis