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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
[Impact of intrauterine infection on long-term brain development of premature rats]
Yun Shang1, Ling Liu, Kun-Feng Cao
1Department of Neonatology, Guiyang Maternal and Child Health Care Hospital, Guiyang, China.
Insights
Intrauterine infection in pregnant rats led to increased fetal brain cell death and impaired long-term cognitive development in offspring. This highlights the critical impact of prenatal infection on neonatal brain health.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Context:
- Intrauterine infection is a significant risk factor for adverse neurodevelopmental outcomes in premature infants.
- Lipopolysaccharide (LPS) is a potent endotoxin that can induce inflammatory responses and mimic intrauterine infection.
Purpose:
- To investigate the long-term effects of intrauterine infection, induced by lipopolysaccharide (LPS), on the brain development of premature rat offspring.
- To assess the impact of varying LPS doses on neural cell apoptosis and cognitive functions.
Summary:
- Pregnant rats received intraperitoneal injections of saline (control) or LPS (0.3 mg/kg or 0.6 mg/kg).
- Placental pathology and fetal brain neural cell apoptosis (TUNEL assay) were examined.
- Premature rat offspring underwent Y-maze testing on postnatal day 42 to evaluate long-term cognitive development and memory retention.
Impact:
- Intrauterine infection significantly increased neural cell apoptosis in fetal brains.
- LPS-induced infection resulted in impaired cognitive functions, evidenced by increased trials to criterion and reduced correct memory retention in the Y-maze test.
- Findings demonstrate a direct link between intrauterine infection and adverse long-term brain development in neonatal rats.
Objective:
To investigate the impact of intrauterine infection induced by LPS injection on long-term brain development of premature rats.
Methods:
Eighteen day-gestation pregnant rats were randomly assigned to a control group receiving an intraperitoneal injection of normal saline, and two infection groups that were intraperitoneally injected with 0.3 mg/kg or 0.6 mg/kg LPS. Twenty-four hours after injection, 7 pregnant rats of each group were sacrificed. The pathological changes of the placenta after hematoxylin and eosin staining were observed under a light microscope. The neural cell apoptosis of fetal brains was examined by the TUNEL assay. The remained pregnant rats were induced to labour before 21 gestation days. The long-term brain development of premature rats was tested with the Y type electric maze on postnatal day 42.
Results:
Obvious pathological changes were observed in the placenta in the infection groups. The apoptotic neural cells in the fetal brain increased in the infection groups compared with that in the control group (32.41+/-5.36 in the 0.3 mg/kg infection group and 66.41+/-7.61 in the 0.6 mg/kg infection group vs 8.00+/-0.36 in the control group; P<0.01). The number of trials to criterion in the Y type maze test in the infection groups was much more than that in the control group [117.8+/-8.7 (0.3 mg/kg infection group) and 194.4+/-13.7 (0.6 mg/kg infection group) vs 56.8+/-3.7 (control group); P<0.01]. The number of correct reactions in memory retaining in the infection groups was lower than that in the control group (0.62+/-0.09 in the 0.3 mg/kg infection group and 0.37+/-0.09 in the 0.6 mg/kg infection group vs 0.92+/-0.06 in the control group; P<0.05).
Conclusions:
Intrauterine infection can cause fetal rats' neural cell apoptosis and affect adversely long-term brain development of neonatal rats.
