Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells

Ganji, Shobha H.; Qin, Shucun; Zhang, Linhua; Kamanna, Vaijinath S.; Kashyap, Moti L.

doi:10.1016/j.atherosclerosis.2008.04.044

Cited by 191 publications

(143 citation statements)

References 32 publications

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“…50 Niacin also reduces endothelial oxidative stress via increasing the cellular content of nicotinamide adenine dinucleotide phosphate (NAD(P)H) and reduced glutathione (GSH) whilst inhibiting reactive oxygen species (ROS) generation in endothelial cells. 51 Based on the subgroup analyses of this study, higher doses of niacin may be associated with a greater effect on endothelial function. This is in line with previous findings on the dose-response pattern of niacin's effect on HDL-C. 52 However, unlike the HDL-C-boosting effect, 53 improvement of FMD by niacin may not be time-dependent, as shown by lack of increase in the effect size in the subgroup of trials with longer durations of follow-up (> 12 weeks).…”

Section: Discussionmentioning

confidence: 86%

Effect of niacin on endothelial function: A systematic review and meta-analysis of randomized controlled trials

Sahebkar

2014

Vasc Med

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Endothelial dysfunction is an independent predictor of incident atherosclerotic cardiovascular disease (ACVD). Niacin possesses high-density lipoprotein (HDL)-elevating, antioxidant and anti-inflammatory properties, all potentially contributing to the amelioration of endothelial function. However, controversies exist among trials reporting the effects of niacin on endothelium-dependent flow-mediated dilation (FMD) as a reliable surrogate of endothelial function. The objective of this study was to assess the effect of niacin on brachial artery FMD using a meta-analysis of available evidence. MEDLINE and Scopus databases were searched for randomized controlled trials investigating the impact of niacin therapy on brachial artery FMD. Meta-analysis of eligible studies was conducted using a random-effects model. Pooled effects were measured by weighted mean difference (WMD) and 95% confidence intervals (CIs). Quality assessment, and subgroup, meta-regression and sensitivity analyses were conducted using standard methods. Among 596 citations, 19 full-text articles were read and seven were found to be eligible for inclusion. Eligible studies involved 441 subjects comprising 228 in the niacin and 213 in the control groups. Niacin therapy significantly improved FMD (WMD: 1.98%; 95% CI: 0.91-3.05%; p = 0.0003) and this effect was robust in the sensitivity analysis. The effect size was greater in the subgroup of studies administering higher doses of niacin (≥ 2000 mg/day) as well as those studies administering niacin for primary prevention of ACVD. Metaregression indicated no association between niacin-induced changes in FMD and changes in plasma HDL-cholesterol, lowdensity lipoprotein-cholesterol or triglycerides. None of the included studies could find any significant effect of niacin on nitroglycerin-mediated dilation. In conclusion, treatment with niacin improves endothelial function.

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Section: Discussionmentioning

confidence: 86%

Effect of niacin on endothelial function: A systematic review and meta-analysis of randomized controlled trials

Sahebkar

2014

Vasc Med

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“…In the same study, niacin also inhibited angiotensin II-induced reactive oxygen species (ROS) production (Ganji et al 2009). These findings indicate for the first time that niacin inhibits vascular inflammation by decreasing endothelial ROS production and subsequent LDL oxidation (Ganji et al 2009). Kaplon et al have recently tested the hypothesis that vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults (Kaplon et al 2014).…”

Section: Niacinmentioning

confidence: 90%

“…Recent studies indicate that niacin increases vascular endothelial cell redox state, resulting in the inhibition of oxidative stress (Kamanna and Kashyap 2008). These effects were investigated by Ganji et al in vitro, who showed that in cultured endothelial cells niacin increases NADPH levels and reduces GSH (Ganji et al 2009). In the same study, niacin also inhibited angiotensin II-induced reactive oxygen species (ROS) production (Ganji et al 2009).…”

Section: Niacinmentioning

confidence: 99%

“…These effects were investigated by Ganji et al in vitro, who showed that in cultured endothelial cells niacin increases NADPH levels and reduces GSH (Ganji et al 2009). In the same study, niacin also inhibited angiotensin II-induced reactive oxygen species (ROS) production (Ganji et al 2009). These findings indicate for the first time that niacin inhibits vascular inflammation by decreasing endothelial ROS production and subsequent LDL oxidation (Ganji et al 2009).…”

Section: Niacinmentioning

confidence: 99%

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Effects of Established Hypolipidemic Drugs on HDL Concentration, Subclass Distribution, and Function

Gomaraschi

Adorni

Banach

et al. 2014

Handbook of Experimental Pharmacology

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“…The ROS induce the expression of adhesion molecules vascular adhesion molecule 1 (VCAM-1) and monocyte chemattranct protein 1 (MCP-1). 26 These changes may induce alterations in the structure and function of endothelial cells and contribute to the initiation of atherosclerosis. 27 …”

Section: Evolution Of Pathogenic Mechanisms Dyslipidaemiamentioning

confidence: 99%

Biochemical mechanisms underlying atherogenesis

PVLN¹,

VS²

2012

JCSR

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Atherosclerosis remains one of the major causes of death and premature disability in developed countries. Though atherosclerosis was formerly considered a bland lipid storage disease, substantial advances in basic and experimental sciences have illuminated the role of endothelium, inflammation and immune mechanisms in its pathogenesis. Current concept of atherosclerosis is that of a dynamic and progressive disease arising from injury to endothelium, also known as endothelial dysfunction and an inflammatory response to that injury. The lesions of atherosclerosis occur principally in large and medium sized arteries. Atherosclerosis affects various regions of the circulation preferentially and can lead to ischemia of heart, brain or extremities resulting in infarction. This produces distinct clinical manifestations depending on the vessel involved. Several predisposing factors to cardiovascular diseases such as diabetes mellitus, hypertension, obesity, infections act as triggers to the development of atherosclerosis by causing endothelial dysfunction and/or promoting inflammatory response. The evolution of pathogenetic mechanisms has passed through various directions such as oxidative stress, inflammation and immune responses. It is now known that all these are not acting independently but are interrelated and getting unified in the current concept of atherogenesis. The following discussion aims at providing an insight into these developments which can help in a better comprehension of the disease and management of its clinical complications.

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Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells

Cited by 191 publications

References 32 publications

Effect of niacin on endothelial function: A systematic review and meta-analysis of randomized controlled trials

Effect of niacin on endothelial function: A systematic review and meta-analysis of randomized controlled trials

Effects of Established Hypolipidemic Drugs on HDL Concentration, Subclass Distribution, and Function

Biochemical mechanisms underlying atherogenesis

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