Alginate has notably diverse pharmacological activities. The present study investigated the anti-inflammatory activity of the guluronate oligosaccharides prepared by oxidative degradation (GOS-OD) from alginate. GOS-OD significantly attenuated the production of nitric oxide (NO), prostaglandin E2 (PGE2), and reactive oxygen species (ROS), the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and the secretion of pro-inflammatory cytokines in lipopolysaccharide (LPS)-activated murine macrophage RAW 264.7 cells. Moreover, GOS-OD potently decreased the binding of LPS to the cell surface and LPS-induced Toll-like receptor 4 (TLR4) and cluster of differentiation (CD) 14 expression. Additionally, GOS-OD could remarkably inhibit the LPS-induced activation of nuclear factor (NF)-κB and mitogen-activated protein (MAP) kinase pathways in RAW 264.7 cells. These results indicate that GOS-OD may reduce the LPS-stimulated inflammatory responses through blocking the activation of NF-κB and MAP kinases, suggesting that GOS-OD may be considered as a potential nutraceutical for inflammation.

Alginate from marine brown algae has been widely applied in biotechnology. In this work, the effects of alginate-derived oligosaccharide (AdO) on lipopolysaccharide (LPS)/β-amyloid (Aβ)-induced neuroinflammation and microglial phagocytosis of Aβ were studied. We found that pretreatment of BV2 microglia with AdO prior to LPS/Aβ stimulation led to a significant inhibition of production of nitric oxide (NO) and prostaglandin E2 (PGE2), expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and secretion of proinflammatory cytokines. We further demonstrated that AdO remarkably attenuated the LPS-activated overexpression of toll-like receptor 4 (TLR4) and nuclear factor (NF)-κB in BV2 cells. In addition to the impressive inhibitory effect on neuroinflammation, we also found that AdO promoted the phagocytosis of Aβ through its interaction with TLR4 in microglia. Our results suggested that AdO exerted the inhibitory effect on neuroinflammation and the promotion effect on microglial phagocytosis, indicating its potential as a nutraceutical or therapeutic agent for neurodegenerative diseases, particularly Alzheimer’s disease (AD).