The anti-inflammatory effect of fucoxanthin is mainly based on modulation of macrophages function. Macrophages are the residents of immune cells in the innate immune system which play an important role in the maintenance of homeostasis by changing their function according to the tissue. As the residence of the immune system, macrophages are a predominant source of proinflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), proinflammatory cytokines [tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and interleukin-1 ß (IL-1ß)], and ROS (Block et al., 2007). It has been consistently demonstrated that the origin of cancer was at sites of chronic inflammation, in part based on the hypothesis that some classes of irritants, together with the tissue injury and ensuing inflammation they cause, enhance proliferation. Chronic inflammation may also play significant role in mediating neurodegenera-tive diseases such as Parkinson's disease (PD), AD, multiple sclerosis (MS), and acquired immune deficiency syndrome (AIDS) dementia complex (Kim and Joh, 2006).
Secondary metabolites derived from marine algae are known to have promising anti-inflammatory activities (Abad et al., 2008). However, the scientific analysis of anti-inflammatory activity of fucoxanthin has been poorly carried out, and until now, only few studies were reported. Fuco-xanthin is recently known to be a potent anti-inflammatory agent in vitro and in vivo in responses to bacterial lipopolysaccharides (LPS). Shiratori et al. reported that anti-inflammatory effect of fucoxanthin is comparable with predinisolone, a commercially available steroidal anti-inflammatory drug (Shiratori et al., 2005). More recently, Heo et al. screened inhibitory effect of NO production from nine species of brown algae and confirmed that inhibition of NO production correlates with fucoxanthin contents (Heo et al., 2010). In addition, Heo et al. also demonstrated anti-inflammatory effect of fucoxanthin isolated from Myagropsis myagroides in LPS-stimulated RAW 264.7 cells. Fucoxanthin treatment attenuates the productions of NO and PGE2 by inhibiting inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions. The release and expression levels of inflammatory cytokines (TNF-a, IL-6, and IL-1 p) were attenuated by fucoxanthin in a dose-dependent fashion. The anti-inflammatory activities of fucoxanthin were due to the suppression of nuclear factor-kB (NF-kB) and the phosphorylation of mitogen-activated protein kinases (MAPKs; Kim et al., 2010). Production of proinflammatory mediators has been continuously reported in many inflammatory tissues, along with increased expression of their mRNAs and proteins. Therefore, inhibition of proinflammatory mediators by fucoxanthin suggests its potential for the treatment of inflammatory and other related diseases.
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