摘要
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 7d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 .0 5 ) ;②HI后 2周和 3周时脑组织Caspase - 3平均光密度值(0 .39± 0 .0 4 ,0 .38± 0 .0 4 )明显高于相应假手术组 (0 .36± 0 .0 1,0 .36± 0 .0 2 ) ,差异有显著性 (P <0 .0 5 ) ;③bFGF组于治疗 3周后Caspase- 3平均光密度值 (0 .36± 0 .0 9)低于对照组 (0 .37± 0 .0 4 )和HIBD组 (0 .38± 0 .0 4 ) ,差异有显著性 (P <0 .0 5 ) ;④bFGF治疗 3周后TUNEL阳性细胞数 (4 .2 0± 1.30 )亦明显少于对照组 (9.80± 1.92 )和HIBD组 (8.0 0± 1.0 0 ) ,差异有显著性 (P <0 .0 5 )。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.
出处
《中国当代儿科杂志》
CAS
CSCD
2003年第4期335-338,共4页
Chinese Journal of Contemporary Pediatrics
