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Nutrition and Disease

Anthocyanins Inhibit Nuclear Factor-B Activation in Monocytes and Reduce Plasma Concentrations of Pro-Inflammatory Mediators in Healthy Adults^1–3,

⁴ Department of Nutrition, and ⁵ Department of Biostatistics, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway N-0316 and ⁶ Department of Medical Genetics and ⁷ Research Centre, Ullevaal University Hospital, Oslo, Norway N-0407

^* To whom correspondence should be addressed. E-mail: rune.blomhoff{at}medisin.uio.no.

The transcription factor nuclear factor-B (NF-B) is activated by oxidative stress and pro-inflammatory stimuli and controls the expression of numerous genes involved in the inflammatory response. Dampening NF-B activation and thereby limiting the inflammatory response have been suggested as a potential strategy to prevent chronic inflammatory diseases. In cultured monocytes, anthocyanins isolated from bilberries and black currants (Medox) efficiently suppressed LPS-induced activation of NF-B. Furthermore, we studied the effect of anthocyanin supplementation (Medox, 300 mg/d for 3 wk) in a parallel-designed, placebo-controlled clinical trial (n = 120 men and women aged 40–74 y). Differences were observed in several NF-B related inflammatory mediators in the Medox group compared to placebo. The changes in the NF-B-controlled pro-inflammatory chemokines IL-8, "regulated upon activation, normal T cell expressed and secreted," (RANTES) and IFN (an inducer of NF-B activation) in the Medox group (45, 15, and 40% decreases from baseline, respectively) differed from those in the placebo group (20, 0, and 15% decreases from baseline, respectively) (P < 0.050). Similarly, changes in IL-4 and IL-13, 2 cytokines that mediate pro-inflammatory responses and induce NF-B activation, in the Medox group (60 and 38% decreases from baseline, respectively) tended to differ from those in the placebo group (4 and 6% decreases) (P = 0.056 and, P = 0.089, respectively).These data suggest that anthocyanin supplementation may have a role in the prevention or treatment of chronic inflammatory diseases by inhibition of NF-B transactivation and deceased plasma concentrations of pro-inflammatory chemokines, cytokines, and inflammatory mediators.

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