维甲酸、癌性促凝物及肿瘤坏死因子对血管内皮细胞抗凝及纤溶功能的影响  

INFLUENCE OF RETINOIC ACID, CANCERPROCOAGULANT AND TUMOUR NECROSIS FACTORQON THE ANTICOAGULANT AND FIBRINOLYTICFUNCTIONS OF VASCuLAR ENDOTHELIAL CELLS

作　　者：夏利军[1] 储小红[1] 万海英[1] 阮长耿[1] 

机构地区：[1]苏州医学院血栓与止血研究室

出　　处：《中华血液学杂志》1994年第9期461-463,共3页Chinese Journal of Hematology

摘　　要：本研究显示维甲酸（ＲＡ）能明显增加人脐带血管内皮细胞（ＨＵＶＥＣｓ）血栓调节蛋白（ＴＭ）、组织纤溶酶原激活物（ｔ－ＰＡ）和前列环素（ＰＧＩ＿２）的分泌与合成，此种作用呈现时间及剂量依赖性。ＲＡ作用２４小时后可使ＴＭ及ＰＧＩ＿２分泌较初始分别增加３～４倍及７倍左右。癌性促凝物（ＣＰ）与肿瘤坏死因子（ＴＮＦα）作用类似。对ＴＭ呈现抑制作用，对ｔ－ＰＡ及ＰＧＩ＿２则有促进分泌与合成的作用，其中以ＣＰ为明显。ＣＰ尚有抑制ｖＷＦ的作用。联合ＲＡ与ＣＰ或ＴＮＦα一起培养，ＲＡ可逆转后二者对ＴＭ的抑制作用，改变ＣＰ对ｔ－ＰＡ及ｖＷＦ的影响。he arudy demonstrated that retinoic acid (RA) couldincrease the expression of thrombomedulin (TM),prostacylin (PGI_2) and tissue plasminogen activator (t-PA) in human umbilical vein endothelial cells(HUVECs) in vitro. The effects of RA on TM, PGI_2and t-PA were dose and time dependent. The TM andPGI_2 began to increase in 30 minutes after addition ofRA and were 3-4 times and 7 times higher respectivelythan that of untreated control at the 24th hour. It alsoshowed that cancer procoagulant (CP) from acuteleukemia as well as tumour necrosis factor a (TNFα)could suppress the expression of TM secreted by HU-VECs. Both CP and TNFα couid stimulate the preduc-tion of t-PA. RA could reverse the down-regulations ofTM induced by CP and TNFa in HUVECs and changethe influence of CP on vWF and t-PA.

关 键 词：维甲酸 血管内皮细胞 白血病 药理 

分 类 号：R979.1[医药卫生—药品]