Changes of Bcl-2 and Bax expression in white matter of fetal rats after maternal endotoxin administration
- VernacularTitle:内毒素致胎鼠脑白质损伤后Bcl-2和Bax蛋白表达的研究
- Author:
Lingxiang YU
;
Xianghong LI
;
Lin HAN
- Publication Type:Journal Article
- Keywords:
White matter damage;
Intrauterine infection;
Rat;
Apoptosis;
Bcl-2;
Bax
- From:
Chinese Pediatric Emergency Medicine
2008;15(5):451-454
- CountryChina
- Language:Chinese
-
Abstract:
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. Immunohistochemical 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 niter 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 increased 2 h and reached a peak at 12 h. Between the endotoxin-gronp 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 eatablish intrauterine irfection 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 pro-tein. The ratio of Bax to Bcl-2 may play an important role for apoptosis in the lesion of the white matter.
