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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.