摘要
目的探讨内毒素致胎鼠脑白质损伤后凋亡蛋白Bcl-2、Bax的表达及其意义。方法孕鼠随机分为两组：感染组和对照组。感染组：建立宫内感染的动物模型。孕鼠怀孕15d腹腔注射内毒素；对照组：孕鼠怀孕15d腹腔注射生理盐水。分别于给药后2、4、12、24、72h剖腹取胎鼠，取脑组织行组织病理学检查，观察胎盘及胎鼠脑组织病理特点，用免疫组织化学方法检测胎鼠脑组织凋亡蛋白Bcl-2、Bax的表达。结果感染组胎盘组织见中性粒细胞浸润，胎鼠脑组织病理改变包括脑白质染色减淡，结构疏松等。感染组胎鼠脑组织凋亡蛋白Bcl-2的表达自2h开始逐渐下降，而Bax的表达自2h逐渐升高，均于12h达到峰值。2h感染组Bcl-2、Bax的阳性细胞百分数与对照组相比，差异无显著性（P〉0．05）；而4h、12h、24h和72h感染组与对照组相比，差异有非常显著性（P〈0．01）。感染组Bax与Bcl-2的比值均明显高于对照组。在各观察时间点两组相比，差异有非常显著性（P〈0．01）。结论内毒索诱导是制备胎鼠脑白质损伤的一种有效形式。在胎鼠脑白质损伤中Bcl-2可能抑制细胞凋亡，Bax可能诱发细胞凋亡，两者的比率变化可能对脑白质损伤后细胞凋亡的调节起重要作用。
Objective To investigate the changes of Bcl-2 and Bax expression in white matter of fetal rats after maternal endotoxin administration. Methods Pregnant rats were randomly divided into two groups： infection group and control group. The infection group was established by intraperitoneal injection of endotoxin in pregnant rats when gestation was 70% complete （15 days）. The control group was treated with normal saline. The fetal rats were killed at 2, 4, 12, 24 and 72 hours after maternal endotoxin administration. The pathological changes in placenta and in fetal rat brain were determined by HE staining. Immunohistoehemieal method was used to detect the expression of Bcl-2 and Bax proteins in fetal rat brains. Results The major pathological changes in fetal rats after maternal endotoxin administration included neutrophil infiltration in the placenta, weak staining of white matter and focal infarction. After maternal endotoxin administration, the expression of Bcl-2 gradually decreased from 2 h and arrived at the valley at 12 h, while that of Bax gradually in- creased 2 h and reached a peak at 12 h. Between the endotoxin-group and the control group, the number of positive cells of Bcl-2 and Bax in brain of the fetal rat had significant difference at 4, 12, 24 and 72 hours （P〈 0.01 ）, and there was no significant difference at 2 h （P 〉 0.05）. The ratio of Bax to Bcl-2 in the endotoxingroup was significantly higher than that in the control group at each time point （P〈0.01）.Conclusion Endotoxin can be used to establish intrauterine infection models and the infection may cause damage to the white matter. Overexpression of Bcl-2 protects cell from apoptosis, but Bax may function as a cell death effector protein. The ratio of Bax to Bcl-2 may play an important role for apoptosis in the lesion of the white matter.
出处
《中国小儿急救医学》
CAS
2008年第5期451-454,共4页
Chinese Pediatric Emergency Medicine
