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作 者:杨晓鲲[1] 郑峻松[1] 张新[1] 蒲晓允[1]
机构地区:[1]第三军医大学新桥医院检验科,重庆400037
出 处:《第三军医大学学报》2006年第18期1837-1839,共3页Journal of Third Military Medical University
摘 要:目的探讨糖皮质激素诱发型TNF受体(glucocorticoid-induced tumor necrosis factor receptor,G ITR)的抗体对抗小鼠L615白血病(T淋巴细胞来源白血病)的效果和作用机制。方法以L615小鼠建立白血病模型,分3组实验组以及阴性对照组,观察实验小鼠生存状态及时间、外周血白细胞计数及分类、外周血和骨髓中白血病细胞形态变化、肝脾指数、肝脾组织病理改变。结果G ITR抗体可以延长L615白血病小鼠的生存时间,可引起骨髓中白血病细胞发生凋亡、坏死、肝脾指数降低、肝脾组织被白血病细胞浸润,提示G ITR抗体能够降低和缓解白血病细胞所致的小鼠外周血白细胞的升高和浸润,以及肝脾的肿大。结论通过免疫调节机制G ITR抗体能够有效地抑制L615白血病细胞的增殖,进而抑制白血病的发展。Objective To investigate the effect and the mechanism of the GlTR-antibody (glucocorticoidinduced tumor necrosis factor receptor-ligand antibody) on the mouse leukemia model induced by L615. Methods The mouse leukemia models induced by L615 cells were divided into 4 groups: negative controls (peritoneal injection of normal saline, 0.2 ml/d), GITR group ( GITR, 100, infused through caudal vein 2 d before leukemic lymphocytes inoculation, again at dose of 50 μg/each mouse after inoculation), Cyclophosphamide group (200 mg · kg^-1 · d^-1 , intraperitoneal injection from the 3^rd day after inoculation for 3 d) , GITR + Cyclophosphamide group (100 mg · kg^-1 · d^-1 Cyclophosphamide instead). The survival time,leukocyte counting in the peripheal blood, liver and spleen index were calculated and the pathological examination of liver, spleen were performed. Results GITR-ligand could prolong the survival time of mouse leukemia model, lead the necrosis and apoptosis of leukemic cells in bone marrow, decrease the liver and spleen index, decrease and relieve the leukocyte increase of peripheal blood and the irregular swelling of liver and spleen. Conclusion Through immunoregulation, GlTR-antibody can inhibit the L615 leukemic cells effectively,therefore inhibit the progress of leukemia to some extent.
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