Anthocyanins Inhibit Nuclear Factor-B Activation in Monocytes and Reduce Plasma Concentrations of Pro-Inflammatory Mediators in Healthy Adults.
Anette Karlsen4, Lars Retterstøl6, Petter Laake5, Ingvild Paur4, Siv Kjølsrud-Bøhn4, Leiv Sandvik7 and Rune Blomhoff4,*
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
The transcription factor nuclear factor-B (NF-B) is activatedby oxidative stress and pro-inflammatory stimuli and controlsthe expression of numerous genes involved in the inflammatoryresponse. Dampening NF-B activation and thereby limiting theinflammatory response have been suggested as a potential strategyto 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-controlledclinical trial (n = 120 men and women aged 40–74 y).
Differenceswere observed in several NF-B related inflammatory mediatorsin the Medox group compared to placebo. The changes in the NF-B-controlledpro-inflammatory chemokines IL-8, "regulated upon activation,normal T cell expressed and secreted," (RANTES) and IFN(aninducer of NF-B activation) in the Medox group (45, 15, and40% decreases from baseline, respectively) differed from thosein the placebo group (20, 0, and 15% decreases from baseline,respectively) (P < 0.050).
Similarly, changes in IL-4 andIL-13, 2 cytokines that mediate pro-inflammatory responses andinduce NF-B activation, in the Medox group (60 and 38% decreasesfrom baseline, respectively) tended to differ from those inthe placebo group (4 and 6% decreases) (P = 0.056 and, P = 0.089,respectively).These data suggest that anthocyanin supplementationmay have a role in the prevention or treatment of chronic inflammatorydiseases by inhibition of NF-B transactivation and deceasedplasma concentrations of pro-inflammatory chemokines, cytokines,and inflammatory mediators.