咖啡酸对阿糖胞苷致小鼠白细胞、血小板减少及血小板体积变化的预防和治疗作用

目的:观察咖啡酸对阿糖胞苷(Ara-C)诱发小鼠白细胞、血小板减少及血小板体积(MPV)变化的影响。方法:参照徐国良等方法诱发Ara-C致小鼠白细胞、血小板减少及MPV 变化模型, 分为咖啡酸600、 300、 150 mg/kg^-1·d^-1 剂量组、复方阿胶浆组(阳性对照组)、模型对照组、正常对照组。小鼠给Ara-C 造模同时连续灌胃用药12 d, 分别于给药6、 8、 10、 12 d 自小鼠尾部取血检测白细胞计数(WBC)、血小板计数(PLT)及MPV, 观察咖啡酸对小鼠白细胞及血小板的预防和治疗作用。结果:咖啡酸300 mg/kg^-1·d^-1 组给药6 dWBC 为4. 8 ±1. 2, 600、 300 mg/kg^-1·d^-1剂量组给药10 d WBC 为(909 ±179)、(1056 ±135)×10⁹/L;咖啡酸各剂量组给药12 d MPV 分别为(6. 00 ±0. 23)、(5. 90 ±0. 20)和(6. 03 ±0. 21)fL, 与模型对照组比较差异有统计学意义(P <0. 05)。结论:咖啡酸可用于治疗临床化疗后引起的白细胞及血小板减少, 保护血小板的损伤。

Preventive and therapeutical effects of caffeic acid on leucopenia and thrombocytopenia and MPV change induced by cytosine arabinoside in mice

AIM:To observe the effect of caffeic acid on leucopenia, thrombocytopenia and platelet volume changes induced by cytosine arabinoside (Ara-c) in mice. METHODS:The leucopenia and thrombocytopenia and platelet change model was established by administration of ara-C in mice. The mice were divided into different groups treated by various dose of caffeic acid (600, 300 and 150mg/kg^-1·d^-1), positive control group (gelatina nigra compound), model control and normal control group. The mice were administration cytosine arabinoside and caffeic acid synchronally and the number of white blood cell and blood platelet number was counted and blood platelets volume was compared at regular time (6, 8, 10, 12 d followed administration of caffeic acid)to evaluate the effects of caffeic acid. RESULTS:After administration of caffeic acid at dose of 300 mg/kg^-1·d^-1 for 6 d, the white cell number is (4. 8 ±1. 2)×10⁹/L. After administration of caffeic acid at dose of 600mg/kg^-1·d^-1 and 300 mg/kg^-1·d^-1 for 10 d, the platelet count number is (909 ±179)and (1056 ± 135)×10⁹/L, and after 12 d administration, the platelet volume is (6. 00 ±0. 23), (5. 90 ±0. 20)and (6. 03 ±0. 21)fL, respectively. There were statistical significances between compare group with model control (P <0. 05).CONCLUSION:Caffeic acid can be used for curing leucopenia and thrombocytopenia induced by chemotherapy and protecting platelet from injury.