Table 1.

Anti-inflammatory potential of fucoidan purified from marine algae.

Study	Cell Line	Concentration	Algal Species and Fucoidan Purified	Cell Signaling Activity	Reference
Inflammatory related cytokine modulation and expressing anti-obesity effects	3T3-L1	1–100 µg/mL	Undaria pinnatifida Polysaccharides (≈60%) and sulfate (≈25%) with less protein content	Significantly decrease the expression of inflammation-related genes during adipogenesis in 3T3-L1 adipocytes. Adipogenesis major markers (c/EBPα, PPARγ) were down regulated via fucoidan. Inactivation of aP2 led to the weakening of TNF-α, MCP-1, PA-1 levels. Lipid accumulation and ROS content in adipocytes were attenuated by fucoidan.	Kim et al. (2012) [52]
Fine dust (FD) induced inflammatory responses in HaCaT keratinocytes are ameliorated by fucoidan	Human skin keratinocytes (HaCaT)	12.5–100 µg/mL	Sargassum horneri purified fucoidan fraction SHC4-6 was reported as a highly sulfated mannofucan (≈45 kDa)	SHC4-6 dose-dependently lowered ROS levels in Fine Dust-induced HaCaT keratinocytes, also downregulated inflammatory cytokines, tumour necrosis factor-α, interleukin (IL)-1β, -5, -6, -8, -13, interferon-γ, and chemokines, macrophage-derived chemokine, eotoxin, and thymus and activation regulated chemokine. Molecular mediators of MAPK and NF-κB pathway were downregulated by SHC4-6. This could successfully recover the impact of FD on skin barrier molecular mediators.	Fernando et al. (2021) [2]
LPS induced inflammation in macrophages is attenuated by fucoidan from Sargassum swartzii	RAW 264.7 macrophage cells	25–200 µg/mL	Fucoidan fraction F4 composed of Polysaccharide (approximately 60%), Sulfate (approximately 33.99%) with a low amount of Protein (0.41%) and Polyphenols (0.32 %)	Significantly decrease the NO production stimulated by LPS and also downregulate the expression of inflammatory mediators such as iNOS and COX-2 including pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), with a dose-dependent manner. The anti-inflammatory effect was exhibited via the suppression of TLR mediated MyD88, IKK complex ultimately blocking NF-κB and MAPK activation.	Jayawardena et al. (2020) [5]
Inflammatory responses stimulated via LPS in macrophages are inhibited via Padina commersonii purified fucoidan	RAW 264.7 macrophage cells	25–100 µg/mL	Purified fucoidan was rich in fucose and sulfate. Composed of 76.57 ± 2.54% polysaccharides and 11.20 ± 0.10% sulfates. FTIR results demonstrated structural similarity with commercial fucoidan.	Significantly down-regulated LPS-activated mRNA and protein expression levels of TLR2, TLR4, and MyD88 which are the inducers of NF-κB transcriptional factors via blocking TLR/MyD88/NF-κB signal transduction.	Sanjeewa et al. (2019) [39]
Anti-inflammatory effects of Sargassum horneri were evaluated in RAW 264.7 macrophages and zebrafish model	RAW 264.7 macrophage cells	12.5–50 µg/mL	A fucoidan (SHCF2) was purified via enzyme assisted extraction and FPLC system. Composed of polysaccharides (approximately 65%) and sulfate (approximately 12.5%) with protein (approximately 14%)	Inhibited the LPS-stimulated NO production in RAW 264.7 cells (IC50 = 40 μg/mL) via the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signal pathways. Specifically, SHCF2 down-regulated the heart-beating rate, cell death, ROS, and NO levels in LPS-exposed zebrafish embryo.	Sanjeewa et al. (2019) [62]
Potential molecular mechanisms of fucoidan from Saccharina japonica is evaluated against LPS induced macrophages	RAW 264.7 macrophage cells	50–200 µg/mL	Fraction 6 (SF6) Composed of polysaccharides approximately 58%) and sulfate (approximately 36%) with low amount of protein (approximately 1%)	SF6 remarkably inhibited LPS-induced production of various inflammatory mediators and pro-inflammation cytokines, including nitric oxide (NO), NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-β (IL-β), and interleukin-6 (IL-6). A mechanism study showed that SF6 could effectively inhibit inflammatory responses through blocking LPS-induced inflammation pathways, including nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and Janus kinase (JAK)-2 and signal transducer and activator of transcription (STAT)-1/3 pathways.	Ye et al. (2020) [70]