Ascorbic Acid and Atherosclerotic Cardiovascular Disease

Lynch, Shaina M.; Gaziano, J. Michael; Frei, Balz

doi:10.1007/978-1-4613-0325-1_17

Cited by 45 publications

(31 citation statements)

References 123 publications

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“…However, it must be noted that others have also shown that vitamin C can also suppress HIV expression in an NF-B-independent manner (43). Other NF-B-dependent pathologies in which beneficial effects for vitamin C have been claimed include cardiovascular disease (7,16) and cancer (6, 10 -13).…”

Section: Discussionmentioning

confidence: 99%

“…The current recommended dietary allowance (1) for vitamin C is 60 mg/day for nonsmoking adult males, which is sufficient to prevent scurvy (5). However, vitamin C has been suggested as having both a preventative and therapeutic role in a number of other pathologies when administered at much higher-than-recommended dietary allowance levels, including cancer (6), atherosclerosis (7), and viral infections (8,9).…”

mentioning

confidence: 99%

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Vitamin C Inhibits NF-κB Activation by TNF Via the Activation of p38 Mitogen-Activated Protein Kinase

Bowie

O’Neill

2000

The Journal of Immunology

298

173

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The transcription factor NF-κB is a central mediator of altered gene expression during inflammation, and is implicated in a number of pathologies, including cancer, atherosclerosis, and viral infection. We report in this study that vitamin C inhibits the activation of NF-κB by multiple stimuli, including IL-1 and TNF in the endothelial cell line ECV304 and in primary HUVECs. The induction of a NF-κB-dependent gene, IL-8, by TNF was also inhibited. The effect requires millimolar concentrations of vitamin C, which occur intracellularly in vivo, particularly during inflammation. Vitamin C was not toxic to cells, did not inhibit another inducible transcription factor, STAT1, and had no effect on the DNA binding of NF-κB. Inhibition by vitamin C was not simply an antioxidant effect, because redox-insensitive pathways to NF-κB were also blocked. Vitamin C was shown to block IL-1- and TNF-mediated degradation and phosphorylation of I-κBα (inhibitory protein that dissociates from NF-κB), due to inhibition of I-κB kinase (IKK) activation. Inhibition of TNF-driven IKK activation was mediated by p38 mitogen-activated protein kinase, because treatment of cells with vitamin C led to a rapid and sustained activation of p38, and the specific p38 inhibitor SB203580 reversed the inhibitory effect of vitamin C on IKK activity, I-κBα phosphorylation, and NF-κB activation. The results identify p38 as an intracellular target for high dose vitamin C.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Vitamin C Inhibits NF-κB Activation by TNF Via the Activation of p38 Mitogen-Activated Protein Kinase

Bowie

O’Neill

2000

The Journal of Immunology

298

173

View full text Add to dashboard Cite

show abstract

“…The mechanisms of certain drugs affecting triglyceride metabolism can also be explored (Aggarwal et al, 2005;Aggarwal et al, 2006). However, no advanced atherosclerotic lesions have been observed in guinea pigs (Lynch et al, 1996;Singh et al, 2009), and the literature considering guinea pigs as surrogates to surgical models is quite sparse. Additionally, antibodies for studying the pathways involved in atherogenic inflammation are lacking.…”

Section: Guinea Pigsmentioning

confidence: 99%