Fucoidans are sulfated heteropolysaccharides found in the cell walls of brown seaweeds (Phaeophyceae) and in some marine invertebrates. Generally, fucoidans are composed of significant amounts of L-fucose and sulfate groups, and lesser amounts of arabinose, galactose, glucose, glucuronic acid, mannose, rhamnose, and xylose. In recent years, fucoidans isolated from brown seaweeds have gained considerable attention owing to their promising bioactive properties such as antioxidant, immunomodulatory, anti-inflammatory, antiobesity, antidiabetic, and anticancer properties. Inflammation is a complex immune response that protects the organs from infection and tissue injury. While controlled inflammatory responses are beneficial to the host, leading to the removal of immunostimulants from the host tissues and restoration of structural and physiological functions in the host tissues, chronic inflammatory responses are often associated with the pathogenesis of tumor development, arthritis, cardiovascular diseases, diabetes, obesity, and neurodegenerative diseases. In this review, the authors mainly discuss the studies since 2016 that have reported anti-inflammatory properties of fucoidans isolated from various brown seaweeds, and their potential as a novel functional material for the treatment of inflammatory diseases.

The ocean is a valuable natural resource that contains numerous biologically active compounds with various bioactivities. The marine environment comprises unexplored sources that can be utilized to isolate novel compounds with bioactive properties. Marine cyanobacteria are an excellent source of bioactive compounds that have applications in human health, biofuel, cosmetics, and bioremediation. These cyanobacteria exhibit bioactive properties such as anti-inflammatory, anti-cancer, anti-bacterial, anti-parasitic, anti-diabetic, anti-viral, antioxidant, anti-aging, and anti-obesity effects, making them promising candidates for drug development. In recent decades, researchers have focused on isolating novel bioactive compounds from different marine cyanobacteria species for the development of therapeutics for various diseases that affect human health. This review provides an update on recent studies that explore the bioactive properties of marine cyanobacteria, with a particular focus on their potential use in human health applications.

The health benefit of brown seaweeds has been proclaimed for centuries, particularly in Asian countries. A brown seaweed Sargassum horneri has been suggested to have immune-boosting and anti-inflammatory/immune-regulatory effects, but their mechanism is still elusive. This study researches the immunological effect of 70% ethanol extract of S. horneri (SHE) on unstimulated and Con A-stimulated murine splenocytes. When treated alone, SHE had an immune stimulatory effect on CD3e+ CD4+ T-helper cells, CD3e+ CD8+ cytotoxic T cells, CD45+ CD11b+ macrophages, Ly-6C+ Ly-6 G+ granulocytes, and Ly6 G- Ly6Clow eosinophils. Furthermore, SHE enhanced wide spectrum of Th cytokines such as TNF-α, IFN-γ (Th1), IL-4, IL-5, IL-13 (Th2), and IL-6 (Th17), which also stimulated the macrophage polarizing cytokines and enhanced macrophage derived cytokine secretion. SHE in Con A (5 μg/mL) stimulated cells decreased T-helper, cytotoxic T cells, granulocytes, eosinophils, and monocytes. These results signify the potential immuno-modulatory effect of SHE which can be developed as a therapeutic agent in immuno-compromised individuals.

Airborne particulate matter (PM) has become a serious health issue causing pulmonary diseases such as asthma. Due to the side effects and non-specificity of conventional drugs, there is a need to develop natural-product-based alternative treatments. Sargassum horneri is a brown alga shown to have anti-oxidant, anti-inflammatory, and anti-allergic effects. Thus, we sought to determine whether ethanol extract of Sargassum horneri (SHE) mitigates the effect of PM exposure on asthma development. To establish a mouse model of asthma, BALB/c mice were sensitized with ovalbumin (OVA, 10 μg) and challenged with PM (5 mg/m³) for 7 days consecutively. SHE (200, 400 mg/kg), Prednisone (5 mg/kg), or PBS was daily administrated orally before PM exposure. SHE mitigated PM exacerbated dendritic cell activation. More importantly, SHE restrained Th2 polarization by attenuating transcription factors GATA3 and STAT5, which further mitigated the expression of Th2 cytokines interleukin (IL)-4, IL-5, and IL-13 in the lung homogenates of PM-exacerbated asthmatic mice. SHE further attenuated PM-exacerbated eosinophil infiltration in the lung, trachea, and BALF. In addition, SHE markedly mitigated the activation of mast cells and the IgE level in serum. Concomitantly, SHE further restrained the Th17 cell response in PM-exposed allergic mice through attenuating expression of transcription factors RORγT, STAT3 and expression of relevant effector cytokines IL-17a. This resulted in mitigated neutrophil infiltration in the lung. Taken together, SHE significantly suppressed PM-exacerbated hypersecretion of mucus in asthmatic mice. These results suggest that SHE has therapeutic potential for treating PM-exacerbated allergic asthma through concomitantly inhibiting Th2/Th17 responses.