Fucoxanthin inhibits PM2.5-induced inflammatory response in MH-S cells

抄録

Background:

Air pollution has been linked to increasing rates of mortality and morbidity in respiratory and cardiovascular diseases. Particulate matters were the most major source and have been studied extensively. Epidemiological studies have shown that exposure to ambient fine particulate matter (PM2.5) is associated with respiratory diseases. Lung inflammation is a central feature of many pulmonary diseases, which can be induced by PM2.5 exposures. However, the mechanisms underlying PM2.5-induced lung inflammation remain unclear. Fucoxanthin (FX), a natural biologically active substance isolated from Ishige okamurae. Previous studies have shown that FX is an anti-inflammatory, anti-cancer, UV-preventative and anti-oxidative agent. In this study, the anti-PM2.5 induced inflammatory capacity of FX and its molecular mechanisms of action were analyzed in murine alveolar macrophage cell line (MH-S cells).

Methods and results:

Cultured MH-S cells were pre-treated with FX and after exposure PM2.5 to screen the influence of FX on COX-2 and iNOS expression by Western blotting. NO and cytokine in culture medium were measured by Griess reaction and ELISA, respectively. Proteins were detected by Western blotting. In PM2.5 exposure MH-S cells, FX potently inhibited the production of NO, iNOS, COX-2 and inflammatory cytokine production. We found that PM2.5-induced NF-kB activation is regulated through inhibition of STAT1 and STAT3 phosphorylation in response to FX. Additionally, FX caused the induction of HO-1 expression, both of which are involved in the secretion of proinflammatory mediators.

Conclusion:

Our data indicate that FX diminishes the proinflammatory mediators NO and the expression of their regulatory genes, iNOS and COX-2, in PM2.5 exposure MH-S cells by inhibiting STAT1/3 dependent NF-kB activation and inducing HO-1 expression.