目的：观察凋亡相关基因Caspase-3在新生大鼠HIBD晚期的蛋 白表达情况以及碱性成纤维细胞生长因子(bFGF)对其影响。方法：采用新 生大鼠HIBD模型，新生7 d龄Wistar大鼠，随机分成4组：HIBD组、假手术组、对照组(生理 盐水治疗)及bFGF治疗组。分别于缺氧缺血(HI)后2周、3周或4周处死大鼠，用免疫组织化学 染色方法观察脑组织Caspase-3的表达情况，用TUNEL法观察神经细胞DNA断裂情况。 结果：①HI后2周和3周时左脑凋亡细胞数高于假手术组(P<0.05)；②HI后 2周和3周时脑组织Caspase-3平均光密度值(0.39±0.04， 0.38±0.04)明 显高于相应假手术组(0.36±0.01， 0.36±0.02)，差异有显著性(P< 0.05)；③bFGF组于治疗3周后Caspase-3平均光密度值(0.36±0.09)低于对照 组(0.37±0.04)和HIBD组(0.38±0.04)，差异有显著性(P<0.05) ；④bFGF治疗3周后TUNEL阳性细胞数(4.20±1.30)亦明显少于对照组(9.80± 1.92)和HIBD组(8.00±1.00)，差异有显著性(P<0.05)。结论：Caspase-3参与了新生大鼠HIBD过程，并持续活化；bFGF可能通过下调HIBD模型 鼠脑组织中Caspase-3的表达及阻止其随后的DNA断裂，从而发挥其神经保护作用。

OBJECTIVE: To explore the role of Caspase-3 protein and DNA fragmentation at late stage after hypoxic ischemic brain damage (HIBD) and the effect of basic fibroblast growth factor (bFGF) on Caspase-3 expression. METHODS: Seven day old Wistar rats were randomly assigned into HIBD group, sham operated group, normal saline treatment group and bFGF treatment group. Caspase-3 expression of the brain was measured by the immunohistochemical method and DNA fragmentation of neurocytes was detected by TUNEL at 2 w, 3 w or 4 w after hypoxia ischemia (HI). RESULTS: ① The number of the TUNEL positive cell in the HIBD group at 2 w and 3 w after HI was greater than that of the sham operated group (P< 0.05 ). ② The Caspase-3 average OD values of the brain ( 0.39 ± 0.04 , 0.38 ± 0.04 ) in the HIBD group at 2 w and 3 w after treatment were significantly higher than those in the sham operated group ( 0.36 ± 0.01 , 0.36 ± 0.02 ), P< 0.05 . ③The Caspase-3 average OD value in the bFGF group at 3 w after HI ( 0.36 ± 0.09 ) was significantly lower than those in the control group and HIBD group ( 0.37 ± 0.04 , 0.38 ± 0.04 ), P< 0.05 . ④ The number of the TUNEL positive cell in the bFGF group at 3 w after treatment ( 4.20 ± 1.30 ) was significantly less than those in the control group and HIBD group ( 9.80 ± 1.92 , 8.00 ± 1.00 ), P< 0.05 . CONCLUSIONS: Caspase-3 may take part in the pathogenesis of HIBD and keep continuous activation, suggesting a prolonged role for apoptosis in neonatal HIBD. bFGF has neuroprotective effects against neonatal HIBD by down regulating Caspase-3 protein expression and preventing DNA from fragmentation.