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Nutraceutical Apigenin: mechanism of action associated with its anti-inflammatory activity and regulation of dendritic cell metabolism
Journal article   Peer reviewed

Nutraceutical Apigenin: mechanism of action associated with its anti-inflammatory activity and regulation of dendritic cell metabolism

Patrick Moore, Rashida Ginwala, Nikil Revuri, Victoria A Kranz, John D Houle, Zafar K Khan and Pooja Jain
The Journal of immunology (1950), v 198(1_Supplement), pp 219-219.12
01 May 2017
DOI: https://doi.org/10.4049/jimmunol.198.Supp.219.12

Abstract

Abstract Flavonoids have a range of biological activities, including anti-inflammatory, anti-carcinogenic, and neuroprotective effects. Apigenin, one such flavonoid abundant in certain plants, has been employed for centuries in the treatment of Parkinson’s, neuralgia, asthma and other diseases owing to the positive health effects attributed to this group of compounds. Due to Apigenin’s relative abundance and low intrinsic toxicity amongst flavonoids, it can be considered as a potential natural treatment for inflammatory disorders of the central nervous system (CNS), such as multiple sclerosis. However, there is distinct lack of information regarding the molecular mechanism of action of Apigenin leading to its modulatory effects on dendritic cells (DC), a key cell type responsible for maintaining immune balance especially in specialized locations such as the CNS. Here, we investigate the effect of Apigenin on RelB, a NF-kB family protein, which is vital to DC maturation and function. Apigenin reduced cytoplasmic RelB levels in LPS-treated DCs isolated from normal peripheral blood of a healthy donor. Gene and protein expression of downstream targets of RelB activation, IL-12, IL-23, IL-6, IL-1β and TNF-α was also reduced upon Apigenin treatment. Further, RelB is also known to engineer a metabolic switch in immune cells upon inflammation to meet the increased energy requirements. We observed a decrease in glucose uptake and lactate production (glycolysis), and an increase in mitochondrial activity when LPS-induced DCs were treated with Apigenin. These results provide key information about the molecular events controlled by Apigenin in its regulation of DC activity marking its potential as a therapy for neuroinflammatory disease.

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