Religa P, Kazi M, Thyberg J, Gaciong Z, Swedenborg J, Hedin U
Department of Surgical Sciences, Division of Vascular Surgery, SE-171 76 Stockholm, Sweden.
Eur J Vasc Endovasc Surg. 2000 Nov;20(5):419-26. doi: 10.1053/ejvs.2000.1220.
fucoidan has previously been shown to inhibit the proliferation of arterial smooth muscle cells both in animal models and in vitro. However, the mechanisms behind the anti-proliferative effects of this polysulfated polysaccharide are not known in detail. Here, the inhibitory effect of fucoidan on rat aortic smooth muscle cell proliferation was examined and compared with the effects of heparin after stimulation with fetal calf serum, platelet-derived growth factor BB, basic fibroblast growth factor, heparin-binding epidermal growth factor, and angiotensin II.
the cultures were analysed with respect to cell proliferation and DNA synthesis by cell counting and measurement of(3)H-thymidine incorporation. Phosphorylation of mitogen-activated protein kinase and nuclear translocation of phosphorylated mitogen-activated protein kinase were studied by immunoblotting and immunocytochemistry.
fucoidan was shown to be a more potent inhibitor of smooth muscle cell proliferation than heparin. Fucoidan also reduced growth factor-induced activation of mitogen-activated protein kinase and prevented nuclear translocation of phosphorylated mitogen-activated protein kinase.
fucoidan is a more potent anti-proliferative polysulphated polysaccharide than heparin and may mediate its effects through inhibition of the mitogen-activated protein kinase pathway in a similar manner as heparin.
岩藻依聚糖先前已在动物模型和体外实验中显示出抑制动脉平滑肌细胞增殖的作用。然而，这种多硫酸化多糖抗增殖作用背后的机制尚不清楚。在此，研究了岩藻依聚糖对大鼠主动脉平滑肌细胞增殖的抑制作用，并与肝素在胎牛血清、血小板衍生生长因子BB、碱性成纤维细胞生长因子、肝素结合表皮生长因子和血管紧张素II刺激后的作用进行了比较。
通过细胞计数和测量³H-胸腺嘧啶核苷掺入量来分析细胞增殖和DNA合成。通过免疫印迹和免疫细胞化学研究丝裂原活化蛋白激酶的磷酸化和磷酸化丝裂原活化蛋白激酶的核转位。
岩藻依聚糖被证明是比肝素更有效的平滑肌细胞增殖抑制剂。岩藻依聚糖还降低了生长因子诱导的丝裂原活化蛋白激酶的激活，并阻止了磷酸化丝裂原活化蛋白激酶的核转位。
岩藻依聚糖是一种比肝素更有效的抗增殖多硫酸化多糖，可能通过与肝素类似的方式抑制丝裂原活化蛋白激酶途径来介导其作用。
