The Study On Apoptosis In Cerebral White Matter Damage Of Fetal Rats After Maternal Endotoxin Administration

Objective Intrauterine infection is closely related to cerebral white matter damagein premature infants.The study was undertaken to investigate the occurrence of apoptosisand the expression of its related gene (Bcl-2, Bax) in cerebral white matter damage of fetalrats after maternal endotoxin administration, so as to provide the experimental base forfinding clinical treatment of cerebral white matter damage in premature infants.Methods Pregnant rats were randomly divided into two groups:infection group andcontrol group.The infection group was established by intraperitoneal injection ofendotoxin in pregnant rats when gestation was 70% Complete (15 days).The control groupwas treated with normal saline.The fetal rats were killed after maternal endotoxinadministration 2,4,12,24 and 72 hours, respectively. The pathological changes in placentaand in fetal rat brain were determined by hematoxylin and eosin(HE) stain-ing. Immunohistochemical method was used to detect the expression of MBP, Bcl-2 andBax in fetal rat brains. Using transferase-mediated dUTP nick end labeling (TUNEL) toexamine the apoptotic cells.Results After maternal endotoxin administration, infiltration of neutrophil in theplacenta, weak staining of cerebral white matter and focal rarefaction in the fetal rat brainswere observed. Positive staining of MBP in the fetal rat brains after endotoxin injectionwas much less and weaker. In the endotoxin-treated group,the number of positive cells ofBcl-2 gradually decreased and arrived at the valley at the time of 12h,while that of Baxand TUNEL gradually increased and peaked at the time of 12h and 24h,respectively.Theapoptotic index and the ratio of Bax to Bcl-2 in the endotoxin-treated group wassignificantly higher than that in the control group at each time point (p＜0.01).Conclusions Endotoxin can be used to establish intrauterine infection models andthe infection may cause the lesion of the white matter. Cell apoptosis and the expression ofits related gene (Bcl-2, Bax) could be observed in cerebral white matter damage of fetalrats. The ratio of Bax to Bcl-2 may play an important role for apoptosis in the lesion ofthe white matter. Overexpression of Bcl-2 protects cell from apoptosis, but Bax mayfunction as a cell death effector protein.