Anti-inflammatory and Anti-tumor activity of a carotenoid isolated from brown algae through MAPKs regulation

Abstract

Fucoxanthin (FX), a major carotenoid of edible brown algae, has reported to have potent anti-inflammatory and anti-tumor activity both in vitro and in vivo. However, the mechanism underlying FX-induced actions remains unclear. In the present study, we designed to evaluate the molecular mechanism of FX isolated from a marine algae in RAW 264.7 cells for anti-inflammation and against HL-60 and B16F10 cell lines for anti-tumor effects. FX induced dose-dependent reductions in the levels of iNOS and COX-2 proteins and concomitant reductions in the production of NO and PGE2. Additionally, FX was shown to suppress the production of inflammatory cytokines and shown to induce a dose-dependent inhibition of the phosphorylation of mitogenactivated protein kinases (MAPKs JNK, ERK and p38). In case of anti-tumor effect, we found that ROS are generated during FX-induced apoptosis in HL-60 cells, and NAC which is a scavenger of ROS, suppressed FX-induced cytotoxicity and apoptosis. Furthermore, the treatment with NAC dramatically inhibited FX-induced phosphorylation of JNK and p38 kinase in HL-60 cells. Moreover, FX reduced the viability of B16F10 cells in a dose-dependent manner accompanied by the induction of cell cycle arrest during the G0/G1 phase and apoptosis. These findings reveal, in part, the molecular basis underlying the anti-inflammatory and anti-tumor properties of FX.t study, we designed to evaluate the molecular mechanism of FX isolated from a marine algae in RAW 264.7 cells for anti-inflammation and against HL-60 and B16F10 cell lines for anti-tumor effects. FX induced dose-dependent reductions in the levels of iNOS and COX-2 proteins and concomitant reductions in the production of NO and PGE2. Additionally, FX was shown to suppress the production of inflammatory cytokines and shown to induce a dose-dependent inhibition of the phosphorylation of mitogenactivated protein kinases (MAPKs JNK, ERK and p38). In case of anti-tumor effect, we found that ROS are generated during FX-induced apoptosis in HL-60 cells, and NAC which is a scavenger of ROS, suppressed FX-induced cytotoxicity and apoptosis. Furthermore, the treatment with NAC dramatically inhibited FX-induced phosphorylation of JNK and p38 kinase in HL-60 cells. Moreover, FX reduced the viability of B16F10 cells in a dose-dependent manner accompanied by the induction of cell cycle arrest during the G0/G1 phase and apoptosis. These findings reveal, in part, the molecular basis underlying the anti-inflammatory and anti-tumor properties of FX.