Molecular Weight Fucoidan Research Articles

Fucoidan with three functions extracted from Sargassum aquifolium integrated rice-husk synthesis dual-imaging mesoporous silica nanoparticle

In this study, we used the nanoparticle delivery system to reduce the side effect of conventional cancer treatment- radiation therapy and chemotherapy. We used rice husk silicon source mesoporous silica nanoparticle doped in Eu3+ and Gd3+ as the carrier in the delivery system and to enable fluorescence and MRI dual-imaging functions for follow-up therapy. In addition, we choose a popular seaweed extract—fucoidan was extracted from the same brown algae—Sargassum aquifolium collected from Taiwan-Pingtung-Kenting-Chuanfan Rock. In this research, we used acid hydrolysis to prepared two different molecular weight fucoidan, the small molecular fucoidan (Fus) as drug, and the molecular weight approximately 1 kDa fucoidan (Ful) as the nanoparticle gatekeeper, and as targeting molecule for overexpressed P-selectin on the surface of the metastatic tumors. The results of the cell cytotoxicity experiment showed that HCT116 cancer cells have a survival rate of approximately 58.12% when treated with 200 μg/mL fucoidan. Dual-imaging rice husk mesoporous silica nanoparticles (rMSN-EuGd) were modified with 1 kDa fucoidan (Ful) as the gatekeeper and target, and the small molecule fucoidan (Fus) was loaded into nanoparticles (Ful-Fus@rMSN-EuGd) at a concentration of 200 μg/mL. The HCT116 cancer cells had a survival rate of approximately 55.56%. The cell cytotoxicity experiment results show that Ful-Fus@rMSN-EuGd can improve the anticancer effect of fucoidan, and the nanoparticle drug delivery system using fucoidan as a drug, target, and gatekeeper was successfully synthesized.

Degradation of different molecular weight fucoidans and their inhibition of TGF-β1 induced epithelial–mesenchymal transition in mouse renal tubular epithelial cells

In order to investigate the anti-fibrotic effect of different molecular weight (Mw) fucoidans on TGF-β1-induced mouse renal tubular epithelial cell (MTEC) mode. Oxidative degradation method was used to obtain fucoidans with different molecular weights and the reaction time, reaction temperature and the concentration of oxidants were investigated. Cell viability was detected by CCK-8, and EMT markers expression was detected by Western-bolt and Cell immunofluorescence assay. As a result, after chemical analysis of three independent batches of prepared samples, one batch of fucoidan sample (LHX 1–9) which chemical contents are similar but Mw ranging from 3.3 KDa to 49.3 KDa were selected to do further research. We found LHX1 (Mw = 3.3 KDa) and LHX 3–9 (Mw = 6.6 KDa, 8.3 KDa, 11.3 KDa, 14.9 KDa, 25.2 KDa, 35.4 KDa, 49.3 KDa) could resist the TGF-β1-induced depithelial–mesenchymal transition (EMT) by decreased expression of Fn and CTGF and maintained epithelial cell morphology in MTEC. However, the relationship between the Mw of fucoidans and their anti-EMT effect is not simply linear. Among the samples, LHX 1, 5 and 8 showed significant anti-EMT effects than others by de-regulated Fn and CTGF expression on MTEC cells.

Downregulation of Microparticle Release and Pro-Inflammatory Properties of Activated Human Polymorphonuclear Neutrophils by LMW Fucoidan

Exposition of neutrophils (polymorphonuclear neutrophils, PMNs) to bacterial products triggers exacerbated activation of these cells, increasing their harmful effects on host tissues. We evaluated the possibility of interfering with the classic immune innate responses of human PMNs exposed to bacterial endotoxin (lipopolysaccharide, LPS), and further stimulated with bacterial formyl peptide (N-formyl-methionine-leucine-phenylalanine, fMLP). We showed that the low- molecular-weight fucoidan (LMW-Fuc), a polysaccharide extracted from brown algae, attenuated the exacerbated activation induced by fMLP on LPS-primed PMNs, in vitro, impairing chemotaxis, NET formation, and the pro-survival and pro-oxidative effects. LMW-Fuc also inhibited the activation of canonical signaling pathways, AKT, bad, p47phox and MLC, activated by the exposition of PMN to bacterial products. The activation of PMN by sequential exposure to LPS and fMLP induced the release of L-selectin⁺ microparticles, which were able to trigger extracellular reactive oxygen species production by fresh PMNs and macrophages. Furthermore, we observed that LMW-Fuc inhibited microparticle release from activated PMN. In vivo experiments showed that circulating PMN-derived microparticles could be detected in mice exposed to bacterial products (LPS/fMLP), being downregulated in animals treated with LMW-Fuc. The data highlight the autocrine and paracrine role of pro-inflammatory microparticles derived from activated PMN and demonstrate the anti-inflammatory effects of LMW-Fuc on these cells.

Low molecular fucoidan and its macromolecular complex with bee venom melittin

Low molecular weight (LMW) fucoidan, obtained by free radical depolymerization of high molecular polysaccharide extract of brown algae Hizikia fusiformis, was complexed with HPLC purified bee venom melittin. Water soluble form of the LMW fucoidan – melittin complex shows increased anti-inflammatory activity, inhibiting the production of nitric oxide in murine macrophage cell line Raw 264.7. The LMW fucoidan:melitin complex obtained in this study showed good biological activities, resulting in 2-fold reduction of the melittin toxicity. The fucoidan: melittin macromolecular complex obtained should be useful in future therapeutic applications.