白血病患者骨髓中VEGF、bFGF、sICAM-1及CD105表达与髓血屏障调节机制关系研究

Relationship between expression of VEGF,bFGF,sICAM-1 and CD105 and regulation mechanism of cord blood barrier in bone marrow of leukemia patients

目的:探讨白血病患者骨髓中血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)、可溶性细胞间粘附分子-1(sICAM-1)及CD105表达与髓血屏障调节机制的关系。方法:采用ELISA检测63例白血病患者骨髓中VEGF、bFGF、sICAM-1表达,采用原位杂交法,用CD105标记骨髓活化的血管内皮细胞。结果:急性髓系白血病患者VEGF、bFGF、sICAM-1、CD105表达高于对照组,急性淋巴细胞白血病患者中B-ALL的VEGF、bFGF、sICAM-1、CD105表达高于对照组,T-ALL的bFGF、CD105表达高于对照组,差异均具有统计学意义(P<0.05);VEGF、sICAM-1表达与对照组比较,差异无统计学意义(P>0.05);慢性粒细胞白血病患者VEGF、bFGF、sICAM-1、CD105表达高于对照组,差异具有统计学意义(P<0.05);慢性淋巴细胞白血病患者sICAM-1表达高于对照组,差异具有统计学意义(P<0.05),VEGF、bFGF、CD105表达与对照组比较,差异无统计学意义(P>0.05)。结论:骨髓VEGF、bFGF、sICAM-1及CD105表达在不同类型白血病中水平不同,并影响白血病患者髓血屏障的正常调节机制。

Objective and CD105 and regulation m We detected VEGF, bFGF, we also used CD105 to mark To explore the relationship between expression of VEGF, bFGF, sICAM-1 echanism of cord blood barrier in bone marrow of leukemia patients. Methods. sICAM-1 expression in leukemia bone marrow by ELISA in 63 patients. And ： activated endothelial ceils in bone marrow by in situ hybridization. Results.Patients with acute myeloid leukemia had higher VEGF, bFGF, slCAM-1, CD105 expression level than the control group （P%0.05）. Patients with acute lymphoblastic leukemia of B-ALL had higher VEGF, bFGF, sICAM-1, CD105 expression than the control group （P %0.05）. Patients with T-ALL had higher bFGF and CD105 expression level than the control group （P%0.05）. VEGF, sICAM-1 expression level were not significant different from that of the control group （P^0.05）. Patients with chronic myeloid leu- kemia had higher VEGF, bFGF, sICAM -land CD105 expression comparing with the control group （P% 0.05）. Patients with chronic lymphocytic leukemia had higher sICAM-1 expression （P%0. 05）, but VEGF, bFGF, CD105 expression were not significant different from that of the control group （P~ 0.05）. Conclusions： Expression levels of VEGF, bFGF, sICAM-1 and CD105 in bone marrow were differ- ent in various different types of leukemia, which affect the normal regulatory mechanisms in patients with myeloid leukemia blood barrier.