摘要目的 观察慢性苯中毒患者造血抑制期ICBP90的表达及慢性苯中毒患者造血恢复期ICBP90的表达,并探讨慢性苯中毒人群造血抑制与ICBP90的相关性.方法 采集慢性苯中毒患者[包括造血抑制期(13例)、造血恢复期患者(11例)]和健康志愿者(10例)的骨髓,分离单个核细胞,并提取核蛋白.使用免疫印迹法(Western blot)检测核蛋白ICBP90的表达,对慢性苯中毒患者造血抑制和ICBP90表达进行相关性分析.结果 慢性苯中毒造血抑制期患者骨髓单个核细胞中ICBP90表达较正常对照组明显下降,差异有统计学意义(P＜0.01).慢性苯中毒造血恢复期患者骨髓单个核细胞中ICBP90表达较正常对照组明显升高,差异有统计学意义(P＜0.05).慢性苯中毒造血恢复期患者骨髓单个核细胞中ICBP90表达较造血抑制期患者明显升高,差异亦有统计学意义(P＜0.01).慢性苯中毒所致造血抑制患者的ICBP90表达与外周血白细胞、血小板均存在相关性(r1=0.555,P=0.006; r2=0.854,P＜0.01).结论 慢性苯中毒患者造血抑制期ICBP90表达下降,慢性苯中毒患者造血恢复期ICBP90表达增高.慢性苯中毒患者造血抑制与ICBP90具有相关性.

abstractsObjective To observe the change of ICBP90 expression in patients with chronic benzene poisoning and explore the correlation between the expression of ICBP90 and benzene-induced hematotoxicity.Methods The bone marrow samples were from 13 chronic benzene poisoning cases with hematopoietic suppression,11 chronic benzene poisoning cases with hematopoietic regeneration and 10 controls.Western-blot was applied to detect the ICBP90 expression in bone marrow mononuclear cells (BMNCs).The correlation between ICBP90 expression and hematopoietic suppression in patients with chronic benzene poisoning was analyzed.Results The ICBP90 expression of BMNCs in 13 chronic benzene poisoning cases with hematopoietic suppression was significantly lower than that in controls (P＜0.01).The ICBP90 expression of BMNCs in 11 chronic benzene poisoning cases with hematopoietic regeneration was significantly higher than those in controls and 13 chronic benzene poisoning cases with hematopoietic suppression (P＜0.05 or P＜0.01 ),respectively.There were good correlations between the expression of ICBP90 and white blood cell and platelet counts in patients with chronic benzene poisoning (r1=0.555,P=0.006;r2=0.854,P＜0.01).Conclusion The ICBP90 expression of BMNCs in the chronic benzene poisoning cases with hematopoietic suppression decreaswed significantly,and the ICBP90 expression of BMNCs in the chronic benzene poisoning cases with hematopoietic regeneration increased significantly.There was good correlation between hematopoietic suppression and ICBP90 expression in patients with chronic benzene poisoning.