Table 2.
An updated summary of anti-inflammatory activities of fucoxanthin: In vitro and in vivo studies.
| Experimental Model (In Vitro/In Vivo) |
Treatment (Dose, Route, and Duration) |
Major Outcomes | Reference |
|---|---|---|---|
| LPS-activated BV-2 microglia | 5–20 μM (purity ≥ 98%), pre-treatment for 1 h | ↓ IL-6, TNF-α, PGE2, NO, iNOS, COX-2 enzymes; ↑ Nrf-2 activation; ↑ HO-1 expression; ↑ BDNF; ↓ Akt/NF-κB; ↓ MAPKs/AP-1 |
[11] |
| UV-B-stimulated corneal denervation in rats | 0.1 to 10 mg/kg b.w., orally for 6 days | ↑ Nrf2 in cornea; ↓ p38 MAPK; ↓ GFAP-positive neural cells; ↓ TRPV1 expression in the trigeminal ganglia neurons |
[42] |
| LPS-treated mice | 50–200 mg/kg b.w. in 0.5% sodium carboxymethylcellulose, intragastric route for 7 days | ↑ AMPK; ↓ NF-κB; ↓ TNF-α, IL-1β, IL-6; ↓ iNOS and COX-2 |
[41] |
| LPS-induced sepsis mouse model | 0.1–10 mg/kg b.w. extracted from Conticribra weissflogii ND-8, intraperitoneally for 6–120 h; ulinastatin as positive control | ↓ IL-6, IL-1β and TNF-α; | [44] |
| LPS-induced RAW 264.7 cells | 10 nM extracted from Conticribra weissflogii ND-8, co-treatment for 6 h | ↓ NF-κB signaling pathway | |
| Palmitate-activated RAW 264.7 cells | 50 μM (purity ≥ 95%), co-treatment for 12 h | ↓ IL-6, IL-1β, TNF-α and NLRP3 gene; ↑ TGF β gene; ↑ CPT1a, PPAR γ; ↑ pAMPK |
[36] |
| CDAHFD-induced NASH model mice |
0.2%/day extracted from brown seaweed lipid, orally for 4 weeks | ↓ Hepatic IL-1β, IL-6, TNF-α mRNA expression; ↓ MCP-1 mRNA expression; ↓ serum MCP-1 |
[37] |
| UVA-induced reconstructed human skin | all-trans fucoxanthin (0.5% w/v) (purity ≥ 95%) in Alkyl benzoate and ethanol, co-treatment for 15 min; sodium dodecyl sulfate as positive control | ↓ IL-6, IL-8 gene expression | [39] |
| DSS-stimulated ulcerative colitis mice | 50–100 mg/kg b.w., treatment (NA) | ↓ PGE2, COX-2; ↓ NF-κB |
[10] |
| LPS-induced RAW 264.7 macrophages | 4.7–470 ng/mL (purity ≥ 95%) extracted from T. lutea F&M-M36, co-treatment for 18 h; celecoxib 3 μM as positive control |
↓ IL-6; ↑ IL-10, Arg1 |
[38] |
| PM-induced zebrafish embryo | 25–100 μg/mL extracted from Sargassum fusiformis, co-treatment for 72 h | ↓ NO, ROS | [40] |
| PM-activated HaCaT keratinocytes and RAW 264.7 cells | 25–100 μg/mL extracted from Sargassum fusiformis, co-treatment for 30 min | ↓ NO, IL-1β, TNF-α and IL-6; ↓ PGE2, COX-2 and MAPK |
|
| LPS-activated RAW 264.7 cells | 5 μM (purity ≥ 95%), pre-treatment for 12 h | ↓ IL6, IL-1β and TNF mRNA; ↓ TNFα secretion; ↓ PI3K/AKT/ Nrf2 |
[35] |
| LPS/ATP-stimulated BMDMs and BMDCs | 40 μM extracted from Phaeodactylum tricornutum, pre-treatment for 4 h | ↓ IL-1β, IL-6 and TNF-α; ↓ NLRP3, ASC and cleaved caspase-1; ↓ oligomerization of ASC; ↓ NF-κB |
[45] |
| LPS-induced RAW264.7 cells | 2.5 μM (purity ≥ 96%) fucoxanthinol from fucoxanthin, extracted from brown seaweed lipid, co-treatment for 24 h | ↓ proinflammatory mediators; ↓ MAPK/NF-κB signaling pathways |
[46] |
| OVA-triggered asthmatic mice | 10–30 mg/kg b.w. (purity ≥ 95%) in DMSO, intraperitoneally for 28 days; prednisolone 5 mg/kg as positive control | ↓ IL-8, MCP-1 and CCL5; ↓IL-4, IL-5, IL-13; ↑ IFN-γ expression |
[43] |
↑: upregulation; ↓: downregulation.