Effect of simvastatin on monocyte adhesion molecule expression in patients with hypercholesterolemia

Serrano, Carlos; Yoshida, Vanda M.; Venturinelli, Margareth L.; D'Ámico, Elbio Antônio; Monteiro, Hugo P.; Ramires, José Antônio Franchini; Luz, Protásio Lemos da

doi:10.1016/s0021-9150(00)00757-7

Cited by 44 publications

(32 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Anyway, the change in monocyte phenotype followed the lipid-lowering effects of simvastatin and paralleled other anti-inflammatory effects of the drug. This is consistent with a recent finding that patients with hypercholesterolemia have high levels of CD11b and CD14 compared to normolipidemic subjects, which correlated to LDL cholesterol levels and was reversed by simvastatin 20) .…”

Section: Anti-inflammatory Effects Of Simvastatinsupporting

confidence: 93%

Effects of simvastatin on markers of inflammation, oxidative stress and endothelial cell apoptosis in patients on chronic hemodialysis

Kirmizis

Papagianni

Dogrammatzi

et al. 2010

JAT

View full text Add to dashboard Cite

Efstathios Alexopoulos has passed awayAim: We investigated the effects of simvastatin on markers of inflammation, oxidative stress and endothelial cell apoptosis in hyperlipidemic end-stage renal disease patients on chronic hemodialysis (HD). Methods: In 25 hyperlipidemic HD patients who received 10 mg of simvastatin for 6 months and another 25 controls, the extended lipid profile and serum hsIL-6, MCP-1, sICAM-1, sVCAM-1, and sE-selectin, plasma oxLDL, and serum sFas and sFasL levels were determined at baseline, 3 months and 6 months. In 18 patients of the simvastatin group, the expression of CD14, CD16, CD62L and CD64 on monocyfes was determined with flow cytometry. Result: Simvastatin treatment resulted in significant reductions in serum lipid levels at 3 months and beyond, compared to at baseline. Moreover, at 6 months, simvastatin caused a significant reduction in CRP ( p 0.001), which correlated to the decrease in total and LDL cholesterol levels, as well as a significant reduction in IL-6 ( p 0.001), sICAM-1 ( p 0.001), sVCAM-1 ( p 0.001), oxLDL ( p 0.001), sFas ( p 0.02) and CD14 expression ( p 0.001), compared to baseline values. No significant changes in the controls were noticed during the study. Conclusion: In conclusion, in hyperlipidemic HD patients, simvastatin treatment resulted in a significant reduction in markers of endothelial dysfunction, inflammation, oxidative stress, endothelial cell apoptosis and peripheral blood monocyte stimulation. The reduction in CRP appears to be related to the lipid-lowering effects of simvastatin.

show abstract

Section: Anti-inflammatory Effects Of Simvastatinsupporting

confidence: 93%

Effects of simvastatin on markers of inflammation, oxidative stress and endothelial cell apoptosis in patients on chronic hemodialysis

Kirmizis

Papagianni

Dogrammatzi

et al. 2010

JAT

View full text Add to dashboard Cite

show abstract

“…41 Concomitant activation of endothelial cells may occur, making this the first step in the process of atherosclerosis already occurring in the bloodstream in contrast to the present view that atherosclerosis starts by the migration of LDL and TRL-remnants to the subendothelium. 37,[42][43][44] Minimally modified apoB-containing lipoproteins [45][46][47] and postprandial low-density lipoprotein (LDL) particles 48 can activate monocytes. The mechanism of this activation has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

Leukocyte Activation by Triglyceride-Rich Lipoproteins

Alipour

Oostrom²,

Izraeljan³

et al. 2008

ATVB

190

152

View full text Add to dashboard Cite

Objective-Postprandial lipemia has been linked to atherosclerosis and inflammation. Because leukocyte activation is obligatory for atherogenesis, leukocyte activation by triglyceride-rich lipoproteins (TRLs) was investigated. Methods and Results-The expression of CD11b and CD66b after incubation with glucose and native and artificial TRLs (NTRL and ATRL) in vivo and in vitro was evaluated by flowcytometry. Oral fat loading tests showed an increased expression of CD11b on monocytes and neutrophils and CD66b on neutrophils. In 11 volunteers, postprandial leukocytes became enriched with meal-derived fatty acids ([1-13 C]16:0) suggesting uptake of exogenous fat. ApoB binding on leukocytes measured by flowcytometry in 65 subjects was highest on neutrophils and monocytes suggesting adherence of apoB-containing lipoproteins. Physiological concentrations of TRLs showed 62% increased neutrophil CD11b and a dose-dependent increased monocyte CD11b up to 84% in vitro. Incubations with lipid emulsions in the hypertriglyceridemic range showed a 5-fold increased monocyte CD11b expression, which was higher than the positive control (fMLP), and a dose-dependent 2-to 3-fold increased neutrophil CD11b and CD66b. The oxidative scavenger DMTU decreased the neutrophil CD66b expression by 36%. Conclusion-Acute hypertriglyceridemia is a leukocyte activator most likely by direct interaction between TRLs and leukocytes and uptake of fatty acids. TG-mediated leukocyte activation is an alternative proinflammatory and proatherogenic mechanism of hypertriglyceridemia in part associated to the generation of oxidative stress.

show abstract

“…Additionally, some studies have also suggested that the specific statin simvastatin may affect immune-mediated inflammation because of the documented ability of this statin to reduce the adhesion of inflammatory cells to the endothelium, inhibit leukocyte adhesion by direct interactions with the leukocyte-function antigen-1 and modulate the expression of the integrin dimer CD11b on monocytes. Simvastatin may also participate in the regulation of cyFinancial support: CNPq/TWAS, FAPEMIG, ISID/EUAtokine/chemokine gene expression and in the functioning of the innate and adaptive immune systems (Serrano et al 2001, Cui et al 2009, Bu et al 2011.…”

mentioning

confidence: 99%

Short-term therapy with simvastatin reduces inflammatory mediators and heart inflammation during the acute phase of experimental Chagas disease

Silva

Shrestha

Almeida‐Leite

et al. 2012

Mem. Inst. Oswaldo Cruz

View full text Add to dashboard Cite

show abstract

Effect of simvastatin on monocyte adhesion molecule expression in patients with hypercholesterolemia

Cited by 44 publications

References 31 publications

Effects of simvastatin on markers of inflammation, oxidative stress and endothelial cell apoptosis in patients on chronic hemodialysis

Effects of simvastatin on markers of inflammation, oxidative stress and endothelial cell apoptosis in patients on chronic hemodialysis

Leukocyte Activation by Triglyceride-Rich Lipoproteins

Short-term therapy with simvastatin reduces inflammatory mediators and heart inflammation during the acute phase of experimental Chagas disease

Contact Info

Product

Resources

About