Evidence That Niacin Inhibits Acute Vascular Inflammation and Improves Endothelial Dysfunction Independent of Changes in Plasma Lipids

Abstract

Objective-To determine if niacin can confer cardiovascular benefit by inhibiting vascular inflammation and improving endothelial function independent of changes in plasma lipid and lipoprotein levels. Methods and Results-New Zealand white rabbits received normal chow or chow supplemented with 0.6% or 1.2%(wt/wt) niacin. This regimen had no effect on plasma cholesterol, triglyceride, or high-density lipoprotein levels. Acute vascular inflammation and endothelial dysfunction were induced in the animals with a periarterial carotid collar. At the 24-hour postcollar implantation, the endothelial expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and monocyte chemotactic protein-1 was markedly decreased in the niacin-supplemented animals compared with controls. Niacin also inhibited intima-media neutrophil recruitment and myeloperoxidase accumulation, enhanced endothelial-dependent vasorelaxation and cyclic guanosine monophosphate production, increased vascular reduced glutathione content, and protected against hypochlorous acid-induced endothelial dysfunction and tumor necrosis factor ␣-induced vascular inflammation. Conclusion-Previous human intervention studies have demonstrated that niacin inhibits coronary artery disease. Thisbenefit is thought to be because of its ability to reduce low-density lipoprotein and plasma triglyceride levels and increase high-density lipoprotein levels. The present study showed that niacin inhibits vascular inflammation and protects against endothelial dysfunction independent of these changes in plasma lipid levels. Key Words: niacin Ⅲ inflammation Ⅲ endothelial dysfunction N iacin (nicotinic acid) has been used for more than 30 years to treat plasma lipid disorders and to prevent atherosclerotic cardiovascular disease. 1 At pharmacological doses, niacin reduces low-density lipoprotein cholesterol, plasma triglyceride, nonesterified fatty acid, and lipoprotein(a) levels. Niacin also increases the concentration of high-density lipoproteins (HDLs). 2 Human intervention studies have indicated that treatment with niacin, either alone or in combination with other lipid-lowering agents, can slow or reverse the progression of atherosclerosis and reduce cardiovascular event rates and total mortality in patients with hypercholesterolemia and established atherosclerotic cardiovascular disease. 2 In combination therapy with statins, niacin reduces cardiovascular events 3 and slows coronary atherosclerosis progression. 4 It also reduces coronary stenosis progression in patients with metabolic syndrome. 5 It has always been assumed that these beneficial effects are the result of the lipid-modifying effects of niacin.However, recent data have indicated that niacin also decreases C-reactive protein levels, 6 improves endothelial dysfunction, 7,8 increases the endothelial and leukocyte oxidation-reduction (redox) state in vitro, 9 inhibits cytokine-induced monocyte adhesion to human endothelial cells, 9,10 improves plaque stability, and reduces thrombosis. 11 It...

Niacin: Does It affect 8-hydroxy-2-deoxyguanosine levels of the patients having low HDL cholesterol levels?

“…The routine use of early preparations of niacin was limited by side effect profile. Niacin has been superseded in recent years with the advent of newer lipid-modulating interventions [3,4,8]. However, whether niacin itself is used routinely in the future will depend on the outcomes of two large outcome trial (AIM-HIGH and HPS2-THRIVE) [9,10].…”

“…Recent data have indicated that niacin also decreases C-reactive protein levels, improves endothelial dysfunction, increases the endothelial and leukocyte oxidation-reduction (redox) state in vitro, inhibits cytokine-induced monocyte adhesion to human endothelial cells, improves plaque stability, and reduces thrombosis [4,5,6]. Thus, we aimed to evaluate HDL-C and 8-OHdG levels after niacin treatment.…”

Recent advances in the immunology and uterine microbiology of healthy cows and cows that develop uterine disease

“…The mechanism by which NEFAs and BHBA affect the immune system has not been elucidated. Nonetheless, recent research has found that BHBA is a main ligand for the nicotinic acid (Niacin) receptors HM74A (GPR109a) and HM74 (GPR109b) (23,24), and that activation of these receptors, especially HM74A, has widespread anti-inflammatory effects including reduction in leukocyte migration and generation of reactive oxygen species, which has been shown to be beneficial for prevention of atherosclerosis and cardiac disease (25,26) but may be a predisposing factor to uterine disease if a proper inflammatory response is not mounted.…”

Heating Up the Cutaneous Flushing Response

“…1 The mechanisms underlying the antiatherogenic effects of nicotinic acid have been disputed during the past decades, and there is evidence for beneficial effects on plasma lipid levels, as well as for anti-inflammatory effects. [1][2][3][4] Nicotinic acid has been suggested as an addon therapy to the well-established statins for prevention of cardiovascular disease. However, recent clinical data indicate no additional benefit of nicotinic acid treatment in high-risk patients under optimal statin therapy, 5,6 and it is currently only recommended in patients in whom statins cannot be given or do not lead to sufficient changes in plasma lipid levels.…”