A total of 26 species of seaweeds (1 green, 21 brown, and 4 red algae) and 6 polysaccharides were screened for their antihypertensive and antihyperlipidemic activities using rats in order to evaluate their potential application for the prevention of cardiovascular diseases. Although diets containing some pulverized seaweeds moderately elevated total cholesterol (TC), free cholesterol (FC), and low density lipoprotein (LDL), marked antihypertensive and antihypercholesterolemic activities were found in almost all seaweeds, some of which are commonly used as food. In addition, serum levels of high density lipoprotein (HDL) were enhanced 46.0% by seaweed powder diets. Six polysaccharides derived from active 'seaweed species were investigated, and appreciable suppression of hypertension and hypercholesterolemia was observed for all samples. They also markedly enhanced the serum level of HDL.

The data, together with the molecular functions of PIM-1 suggest that PIM-1 may have an important role in CaP progression and has potential to be a diagnostic and prognostic marker for CaP.

Funoran (an algal polysaccharide from Gloiopeltis tenax) significantly inhibited the growth of Ehrlich ascites carcinoma and solid Ehrlich, Meth-A fibrosarcoma, and Sarcoma-180 tumors. In tumor-bearing mice, funoran significantly induced the enhancement of delayed-type hypersensitivity response to sheep red blood cells. When given intraperitoneally, funoran increased the spleen weight of mice. Morphological observations indicated that funoran augmented the transformation from lymphocytes to plasma cells in the spleen. In addition, changes in the T-cell subsets in the spleen, thymus, and peripheral blood were measured by flow cytometry. The results showed that the percentages of L3T4+ and Lyt 2+ T-cells were markedly increased in the peripheral blood. The percentages of asialo CM1+ cells in the thymus and peripheral blood were also significantly increased. Our results suggest that the antitumor effect of funoran is related to the augmentation of T-helper, T-cytotoxic, and NK cells.

Studies were conducted to determine the mechanism of blood pressure-and cholesterol-lowering effects of funoran on rats fed with a saline solution and cholesterol diet. Clofibrate (COIB) was used as a reference hypolipidemic drug. Funoran caused significant reduction of systolic blood pressure (SBP). Funoran and CPIB significantly reduced serum total cholesterol (TC), free cholesterol (FC), triglyceride (TG), LDL-cholesterol (LDL), and atherogenic index (AI) levels in these rats. The increase of sodium, water excretion and sodium-potassium ratio in urine in the funoran group was more significant in the experimental rats thannnnin the control group. Moreover, the ratio of Na and K in serum decreased with the funoran diet. The CPIB diet enhanced cholesterol level in the liver while the funoran diet suppressed the level, but in feces the former diet did not change the cholesterol level while the latter diet increased it. These results suggest that the enhanced ability to excrete sodium in urine by the funoran diet is an important factor for reducing blood pressure and that the antihyperlipidemic effect of funoran was not caused by the mobilization of peripheral cholesterol on the liver, but by the enhanced excretion of cholesterol into feces.