目的：研究表明脑白质损害与少突胶质前体细胞凋亡密切相关，bcl-2蛋白作为抗凋亡蛋白与新生大鼠脑白质损害(WMD)的关系较少报道。该文探讨bcl-2蛋白在新生大鼠脑白质损害(WMD)时的表达变化及意义。方法：将2日龄SD大鼠(n=90)，随机分为两组，实验组(缺氧缺血)45只，对照组(假手术)45只，制成WMD模型；采用TUNEL法测定神经细胞凋亡及免疫组化（SP）法检测bcl-2蛋白在脑室周围白质区不同时间点的表达变化。结果：成功建立了WMD模型。实验组神经细胞凋亡在缺氧缺血后3 d达到高峰，凋亡指数脑白质为37.40±4.26，胼胝体为29.84±1.11，与对照组比较，在4 h，12 h，24 h，3 d，7 d 有统计学意义（P<0.05）。实验组bcl-2蛋白表达在WMD后1 h就上升,12 h达高峰，平均灰度值脑白质为124.96±0.27，胼胝体为130.09±0.77),在1 h，4 h，12 h，24 h，3 d的表达与对照组相比，差异有统计学意义（P<0.05）。结论： 新生大鼠脑白质损害时,bcl-2蛋白早期表达增高，而神经细胞凋亡高峰滞后,二者具有明显时序性，这种时序变化提示bcl-2蛋白可能对神经细胞具有一定保护作用。［中国当代儿科杂志，2007，9（2）：164-168］

OBJECTIVE: Some research has shown that the brain white matter damage is closely related to apoptosis of pre-oligodendrocytes. The relationship of bcl-2 protein, a protein of anti-apoptosis, with brain white matter damage in neonatal rats is rarely reported. This study examined the changes of bcl-2 protein expression following brain white matter damage in neonatal rats. METHODS: Ninety 2-day-old Sprague-Dawley (SD) rats were randomly divided into 2 groups: experimental group (n=45) and control group (n=45).Brain white matter damage was induced by ligation of the right common artery, followed by 6% hypoxia exposure in the rats from the experimental group. The rats of the control group were sham-operated, without hypoxia-ischemia treatment. The expression of bcl-2 protein in the periventricular white matter and the callositas was detected by immunohistochemical technique. Apoptosis of neurocytes in these tissues was detected by TUNEL. RESULTS: The apoptosis index of neurocytes in the experimental group was up-regulated at 4, 12 and 24 hrs and at 3 and 7 days, peaking at 3 days after white matter damage, compared with the control group (P < 0.05). The expression of bcl-2 protein in the experimental group began to increase at 1 hr, reached a peak at 12 hrs and remained a higher level until 3 days after white matter damage compared with that observed in the control group (P< 0.05). CONCLUSIONS: The expression of bcl-2 protein increased at the early stage of white matter damage in neonatal rats. The peak of apoptosis lagged behind that of the bcl-2 protein expression, which suggests that bcl-2 protein may have protective effects against neuronal apoptosis.