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目的观察苯诱发再障模型及氨磷汀干预的病理改变。方法156只雄性CD1小鼠,随机分为6组,1个对照组,1个干预组,4个实验组(B1、B2、B3、B4)。实验组所给苯剂量分别为0．5、1．0、1．5和2．0 ml/kg；对照组单纯注射玉米油；干预组每次给苯半小时前,腹腔注射氨磷汀200 mg/kg。各组均每周3次注射,以玉米油补足4 ml/kg。各实验组分别于给苯前及给苯10、15、20、25次2d后,称重动物,观察小鼠一般情况并检测血象,尸检后取一根股骨、肝和脾,称重并进行组织病理学观察以及增殖细胞核抗原(PCNA)、末端脱氧核甘酸转移酶介导的dUTP缺口末端标记(TUNEL)检测。结果(1)与对照组比较,各实验组小鼠均有部分指标改变,但仅有B4组在给苯25次后全部指标与对照组比较,差异有统计学意义(P＜0．05),B4组体重和脾体比值分别比对照组下降18．51％、63．86％,差异有统计学意义(P＜0．01)；血细胞数目减少,部分骨髓涂片出现油滴,骨髓细胞形态学和组织病理学观察均显示造血细胞减少,非造血细胞增加,肝、脾出现再障的病理改变。(2)干预组与B4(再障)组比较,小鼠一般情况、肝脾和骨髓的病理变化等各项指标均有明显改善,PCNA、TUNEL检测在对照组、B4组和干预组之间差异有统计学意义(P＜0．05)。结论(1)建立苯诱发小鼠再生障碍性贫血模型,可以通过CD1小鼠每周3次皮下注射2 ml/kg苯(共25次)获得。(2)氨磷汀对苯致再障具有一定的保护作用。
Objective To observe the pathological changes of benzene induced aplastic anemia and amifostine intervention. Methods 156 male CD1 mice were randomly divided into 6 groups, 1 control group, 1 intervention group and 4 experimental groups (B1, B2, B3, B4). In the experimental group, the doses of benzene were 0.5, 1.0, 1.5 and 2.0 ml / kg, respectively. The control group was injected with corn oil only. mg / kg. Each group was injected 3 times a week with corn oil to make up 4 ml / kg. Each experimental group was given benzene and benzene for 10,15,20,25 times two days later, the animals were weighed, the general situation of the mice was observed and blood was taken. After the autopsy, a femur, liver and spleen were taken, weighed and carried out Histopathological observation and proliferating cell nuclear antigen (PCNA), terminal deoxyribonucleotidyl transferase mediated dUTP nick end labeling (TUNEL) detection. Results (1) Compared with the control group, some indexes of mice in each experimental group were changed, but there was significant difference between the control group and the B4 group (P <0.05) , The body weight and spleen ratio of B4 group decreased by 18.51% and 63.86% respectively compared with the control group (P <0.01); the number of blood cells decreased and some bone marrow smears showed oil droplets and bone marrow cells Morphological and histopathological observations showed hematopoietic cells decreased, non-hematopoietic cells increased, liver and spleen appeared aplastic pathological changes. (2) Compared with B4 (aplastic anemia) group, the indexes of general condition, pathological change of liver, spleen and bone marrow of mice in intervention group were significantly improved. PCNA and TUNEL detected between control group, B4 group and intervention group The difference was statistically significant (P <0.05). Conclusions (1) The establishment of a benzene-induced aplastic anemia model in mice can be obtained by subcutaneous injection of 2 ml / kg benzene (25 times) three times a week in CD1 mice. (2) Amifostine has some protective effect on benzene-induced aplastic anemia.