Chou Tz-Chong, Fu Earl, Wu Chang-Jer, Yeh Jeng-Hsien
Department of Physiology, National Defense Medical Center, No. 161, Min-Chuan E. Rd. Sec. 6, Taipei, Taiwan, ROC.
Biochem Biophys Res Commun. 2003 Mar 14;302(3):480-3. doi: 10.1016/s0006-291x(03)00173-6.
In this study, chitosan (MW=50,000) was tested for its enhancing platelet activity in rabbit platelet suspensions and the possible mechanisms involved were further investigated. Our results showed that after initial (5 min) and long-term (30 min) contact of platelets with chitosan, the platelet adhesion to chitosan-coated microtiter plates was dose-dependently increased compared to that of solvent control. Similarly, chitosan also dose-dependently increased the platelet aggregation and the intracellular free Ca(2+) rise of Fura-2-AM loaded platelets. Additionally, in the presence of FITC-labeled anti-CD41/CD61, chitosan significantly enhanced the expression of platelet glycoprotein IIb/IIIa complex assayed by a flow cytometer. It is concluded that chitosan is an effective inducer for platelet adhesion and aggregation and the mechanisms of action of chitosan may be associated, at least partly, with the increasing Ca(2+) mobilization and enhancing expression of GPIIb/IIIa complex on platelet membrane surfaces.
在本研究中,测试了壳聚糖(分子量=50,000)对兔血小板悬液中血小板活性的增强作用,并进一步研究了其可能的作用机制。我们的结果表明,血小板与壳聚糖初始接触(5分钟)和长期接触(30分钟)后,与溶剂对照组相比,壳聚糖包被的微量滴定板上的血小板黏附呈剂量依赖性增加。同样,壳聚糖也剂量依赖性地增加了血小板聚集以及Fura-2-AM负载血小板的细胞内游离Ca(2+)升高。此外,在异硫氰酸荧光素标记的抗CD41/CD61存在下,壳聚糖通过流式细胞仪检测显著增强了血小板糖蛋白IIb/IIIa复合物的表达。得出的结论是壳聚糖是血小板黏附和聚集的有效诱导剂,壳聚糖的作用机制可能至少部分与增加细胞内Ca(2+)动员以及增强血小板膜表面GPIIb/IIIa复合物的表达有关。