A new method to label fucoidan sulfate was established with tyramine and fluorescein isothiocyanate isomer I (FITC). Fluorescence spectrophotometry and high performance liquid chromatography verified the successful labelling of fucoidan by FITC. The results of the single-pass intestinal perfusion indicated that the jejunum and ileum are the main absorption sites, and there was carrier saturation. In addition, fucoidan sulfate at 1 mg/ml had no inhibitory effect on Caco-2 cell proliferation. Studies on the transmembrane transport mechanism showed that fucoidan can be absorbed because the apparent permeability coefficient of the drugs (P ) A → B was 3.78 + 0.03 ×10 and that of B → A was 1.42 + 0.19 ×10 . The peak absorption of fucoidan occurred at 120 min after administration; moreover, the higher the concentration used, the worse the absorption was, suggesting the saturation of transport carriers. The absorption was temperature dependent: the absorption at 37°C was much better than that at 4°C. Further, the absorption of fucoidan sulfate might rely on clathrin endocytosis as chlorpromazine (10 μg/ml) significantly inhibited it.

In the present study, we found that PHL, a pepsin hydrolysate of leech with little anti-coagulatory effect, could significantly suppress TNF-α induced mRNA overexpression of endothelial dysfunction-related molecules (ET-1, iNOS, MCP-1, and IL-6). These results provide a reliable experimental basis for identifying new anti-atherosclerosis therapeutics for long term use and with minimal bleeding side effects.

No abstract