肿瘤细胞诱导血小板聚集的机理  

Mechanisms of platelet aggregation induced by tumor cells

作　　者：王兆钺[1] 陈德春[1] 万海英[1] 何杨[1] 阮长耿[1] 黄强[2] 王强[2] 

机构地区：[1]苏州医学院血栓与止血研究室 [2]苏州医学院脑神经研究室

出　　处：《中国病理生理杂志》1991年第1期16-19,共4页Chinese Journal of Pathophysiology

摘　　要：Lewis肺癌细胞(3LL),黑色素瘤细胞(B16a)与绒毛膜上皮癌细胞(NHCh-4)能引起人血小板的聚集反应,但聚集的强度与波型不同。胶质母细胞瘤细胞,(NHC-3)与直肠癌细胞(NHC-6)不引起血小板的聚集反应。抗血小板膜糖蛋白(GP)Ⅱb/Ⅲa的单克隆抗体SZ-21抑制3LL引起的血小板聚集,抗GPIb的单克隆抗体AN51能部分抑制NHCh-4诱导的聚集。NHCh-4能刺激血小板生成TXP_2。3LL与B16a对血小板TXB_2生成的影响很小。结果表明,不同的肿瘤细胞引起血小板聚集的能力和机理各不相同,血小板在不同肿瘤转移中所起的作用也不一样。The rates of human platelet aggregation induced by Lewis lung carcinoma cell line (3LL), melanoma cell line (B(?)εa) and chorioblastoma cell line (NHCh-4) were 16.4±8.1, 12.1±4.1 and 14.3±2.8%, respectively, while glioblastoma cell line (NHC-3) and rectal carcinoma cell line (NHC-6) had not such efficacy. Preincubation of platelets with monoclonal antibody SZ-21 against GPⅡb/Ⅲa blocked 3LL-induced aggregation (P<0.01). Anti-GPⅠb monoclonal antibody AN51 inhibited partially NHCh-4 induced aggregation (P<0.05). Platelet TXB_2 production was markedly stimulated in the presence of NHCh-4, while 3LL or B16a did not influence platelet TXB_2 production. These results indicate that the mechanisms of platelet aggregation induced by different tumor cells are different.

关 键 词：肿瘤细胞 血小板凝集 单克隆抗体 

分 类 号：R730.21[医药卫生—肿瘤]