Yu Hui-min, Yuan Tian-ming, Tang Hong-feng, Li Jian-ping
Children's Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Zhonghua Er Ke Za Zhi. 2003 Dec;41(12):893-6.
To investigate the expression of glial fibrillary acidic protein (GFAP), GFAP mRNA and interleukin-1beta mRNA (IL-1beta mRNA), tumor necrosis factor-alpha mRNA (TNF-alpha mRNA) in neonatal rat brain after intrauterine infection.
Escherichia coli (E. coli) was inoculated into both uterine horns of pregnant rats when gestation was 70% complete (15 days). The control group was treated with normal saline. The pups were killed on the postnatal day 1 (P1), P3 and P7, respectively. The cerebral white matter damage of the neonatal rats was determined by HE staining. Immunohistochemistry was used for evaluation of GFAP expression in neonatal rat brains and RT-PCR to analyze GFAP mRNA, IL-1beta mRNA and TNF-alpha mRNA expression at P1, P3 and P7.
The major histopathological changes in neonatal cerebral white matter at P7 after intrauterine infections were: weak staining of cerebral white matter and focal rarefaction. GFAP-positive cells were observed in both the control and the E. coli-treated groups. The numbers of GFAP-positive cells of the E. coli-treated group pups were markedly increased in periventricular white matter and hippocampus at P7 compared with those of the control group (periventricular white matter: 9.73 +/- 3.55 vs 5.67 +/- 1.90, P < 0.05 and hippocampus: 7.81 +/- 3.61 vs 2.16 +/- 1.11, P < 0.05, respectively). No significantly different levels of GFAP expression in corpus callosum were found between two groups (P > 0.05). The expression of GFAP mRNA in brain of the E. coli-treated neonatal rat was higher than the control at P1, P3 (P1: 0.25 +/- 0.07 vs 0.15 +/- 0.08, P < 0.05 and P3: 0.50 +/- 0.09 vs 0.39 +/- 0.08, P < 0.05, respectively), but the expression of GFAP mRNA in brain of the neonatal rat at P7 had no significant difference between two groups (P > 0.05). The expression of IL-1beta mRNA and TNF-alpha mRNA in brain of the E. coli-treated neonatal rat were higher than of the control at P1 (IL-1beta mRNA: 0.83 +/- 0.19 vs 0.50 +/- 0.30, P < 0.05 and TNF-alpha mRNA: 0.74 +/- 0.30 vs 0.30 +/- 0.20, P < 0.05, respectively), but the expression of IL-1beta mRNA and TNF-alpha mRNA in brain of the neonatal rat at P3 and P7 had no significant difference between two groups (P > 0.05).
The intrauterine infection could cause neonatal white matter damage and IL-1beta, TNF-alpha may be a mechanism mediating between the two events.
探讨宫内感染后新生大鼠脑内胶质纤维酸性蛋白（GFAP）、GFAP mRNA、白细胞介素-1β mRNA（IL-1β mRNA）及肿瘤坏死因子-α mRNA（TNF-α mRNA）的表达。
妊娠70%（15天）时，将大肠杆菌接种于孕鼠双侧子宫角。对照组用生理盐水处理。分别于出生后第1天（P1）、P3和P7处死幼鼠。通过HE染色确定新生大鼠脑白质损伤情况。采用免疫组织化学法评估新生大鼠脑内GFAP表达，采用逆转录-聚合酶链反应（RT-PCR）分析P1、P3和P7时GFAP mRNA、IL-1β mRNA及TNF-α mRNA的表达。
宫内感染后P7时新生大鼠脑白质的主要组织病理学变化为：脑白质染色变淡及局灶性稀疏。对照组和大肠杆菌处理组均观察到GFAP阳性细胞。与对照组相比，P7时大肠杆菌处理组幼鼠脑室周围白质和海马区GFAP阳性细胞数量明显增加（脑室周围白质：9.73±3.55对5.67±1.90，P<0.05；海马区：7.81±3.61对2.16±1.11，P<0.05）。两组胼胝体中GFAP表达水平无显著差异（P>0.05）。大肠杆菌处理的新生大鼠脑内GFAP mRNA在P1、P3时高于对照组（P1：0.25±0.07对0.15±0.08，P<0.05；P3：0.50±0.09对0.39±0.08，P<0.05），但P7时两组新生大鼠脑内GFAP mRNA表达无显著差异（P>0.05）。大肠杆菌处理的新生大鼠脑内IL-1β mRNA和TNF-α mRNA在P1时高于对照组（IL-1β mRNA：0.83±0.19对0.50±0.30，P<0.05；TNF-α mRNA：0.74±0.30对0.30±0.20，P<0.05），但P3和P7时两组新生大鼠脑内IL-1β mRNA和TNF-α mRNA表达无显著差异（P>0.05）。
宫内感染可导致新生大鼠脑白质损伤，IL-1β、TNF-α可能是介导这两个事件的机制。
