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Updated: Jul 15, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Intrauterine infection induced oligodendrocyte injury and inducible nitric oxide synthase expression in the
Ying Shen1, Hui-Min Yu, Tian-Ming Yuan
1Department of Neonatology, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, PR China.
Aims:
In order to investigate the neuropathological effect on the developing rat brain after intrauterine infection, 2', 3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) and inducible nitric oxide synthase (iNOS) were evaluated.
Methods:
Escherichia coli (E. coli) was inoculated into the uterine cervix of the time-pregnant rats and controls were injected with normal saline. Immunohistochemical staining for CNPase was performed to assess oligodendrocyte injury in pup brains at postnatal day 1, 3 and 7 (P1, P3, and P7). Immunohistochemistry was used to evaluate iNOS expression and quantitative reverse transcriptase PCR to analyze iNOS mRNA expression in pup brains at P1, P3 and P7. Nitrate reductase method was used for detection of nitric oxide (NO) concentration in pup brains at P1, P3 and P7.
Results:
The immunohistochemical staining for CNPase in the E. coli-treated group showed a decrease compared with the control in periventricular white matter at P7. Obvious immunohistochemical staining of iNOS was observed in periventricular white matter of the E. coli-treated pup brains at P1. The expression of iNOS mRNA in the E. coli-treated pup brains increased at P1 and P3, but there was no significant difference at P7 compared with controls. Similarly, the NO concentration increased in the E. coli-treated pup brains at P1 and P3, and no significant difference was found at P7 compared with controls.
Conclusions:
The alteration of CNPase expression indicates that intrauterine infection could cause oligodendrocyte injury in the developing brain. Moreover, the increased expression of iNOS followed by the increasing NO concentration after intrauterine infection suggests that iNOS might be a key mediator between the intrauterine infection and oligodendrocyte injury in the developing brain.
