Polygalactan from bivalve Crassostrea madrasensis attenuates nuclear factor-κB activation and cytokine production in lipopolysaccharide-activated macrophage.

A polygalactosamino-glucopyranosyl fucopyranose →4)-β-GlcAp{(3→1)-α-Fucp}-β-GalNAcp-(4,6-SO)-(1→ isolated from the bivalve Crassostrea madrasensis exhibited prospective anti-inflammatory activity against cyclooxygenase-2 and 5-lipoxygenase (IC < 50 μg mL) on lipopolysaccharide-induced macrophages. The polygalactan attenuated inducible nitric oxide synthase (IC 65.7 μg mL) in lipopolysaccharide-prompted inflammation leading to the reduction of pro-inflammatory cytokine nitric oxide (236.2 μg mL lysate), nuclear factor-κB, tumor necrosis factor-α, and interleukins (0.19-0.22 units mg protein at 100 μg mL) by inhibiting cyclooxygenase-2. The polygalacatan suppressed the mRNA of nuclear factor-κB and cyclooxygenase-2 in lipopolysaccharide-induced macrophages. Western blot experiment revealed that the polygalactan attenuated the migration of nuclear factor-κB-p to the nucleus from cytoplasm, and suppressed the phosphorylation of α-subunit of κB inhibitor. Greater selectivity index of sulfated polygalactan (3.93) towards inducible cyclooxygenase-2 as compared with the anti-inflammatory agent ibuprofen (1.11), and the potential to inhibit nuclear factor-κB cascade to generate chemokine production manifested its utilization in the development of functional food attenuating inflammation-related disorders.