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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
[Effect of maternal lipopolysaccharides exposure during pregnancy on vascular structure in neonatal offspring rats]
Shanyu Zhao1, Ya Liu1, Xiaohui Li1
1Department of Pharmaceutics, College of Pharmacy, Third Military Medical University, Chongqing 400038, China.
Insights
Maternal exposure to lipopolysaccharides (LPS) during pregnancy impaired offspring aortic morphology and reduced body weight. Treatment with pyrrolidinedithiocarbamate (PDTC) partially reversed these adverse effects, suggesting a potential therapeutic target.
Area of Science:
- Developmental biology
- Cardiovascular research
- Toxicology
Background:
- Prenatal exposure to inflammatory agents can impact offspring development.
- Lipopolysaccharides (LPS) are potent inducers of inflammation.
- Aortic morphology is critical for cardiovascular health.
Purpose of the Study:
- To investigate the effects of maternal LPS exposure on neonatal rat aortic structure.
- To evaluate the potential protective role of pyrrolidinedithiocarbamate (PDTC) against LPS-induced aortic changes.
Main Methods:
- Pregnant rats were exposed to LPS, LPS + PDTC, or vehicle during gestation.
- Offspring were assessed for body weight, thoracic aortic histopathology, and connexin (Cx) expression (Cx37, Cx40, Cx43, Cx45).
- Techniques included H&E staining, transmission electron microscopy, Real-Time PCR, and confocal microscopy.
Main Results:
- LPS exposure led to reduced offspring body weight and significant aortic lesions, including endothelial dysfunction and vascular smooth muscle cell changes.
- Gap junction numbers and Cx43 expression (mRNA and protein) were decreased in LPS-offspring aortas.
- PDTC treatment partially ameliorated body weight reduction and reversed some of the observed aortic pathology and Cx43 expression changes.
Conclusions:
- Maternal LPS exposure induces detrimental vascular alterations in neonatal offspring.
- These prenatal insults may heighten susceptibility to adult hypertension.
- PDTC demonstrates a partial protective effect against LPS-induced developmental toxicity in the aorta.
Objective:
To explore the role of prenatal exposure to lipopolysaccharides (LPS) on aortic morphology in the neonatal offspring rats.
Methods:
Twelve pregnant rats were randomly divided into three groups: control group, LPS group, and PDTC (pyrrolidinedithiocarbamate, LPS+PDTC) group. The rats were intraperitoneally administered vehicle, LPS (0.79 mg/kg) , or LPS plus PDTC (100 mg/kg) , respectively. LPS was given on the 8th, 10th and 12th days, whereas vehicle and PDTC were given daily from the 8th to the 14th day during gestation. Histopathological alteration of the thoracic aorta was observed by hematoxylin-eosin staining and transmission electron microscopy, thoracic aortic mRNA and protein expression of connexin (Cx) molecules including Cx37, Cx40, Cx43 and Cx45 in offspring was detected by Real Time PCR and confocal laser-scanning microscope, respectively, offspring body weight was measure at day 1 and week 1.
Results:
Body weight at 1 day and 1 week-old offspring was significantly lower in LPS group than in control group (P < 0.01), which were significantly higher in PDTC group compared to LPS group (P < 0.01): [1 day: control group (7.425 ± 0.146) g, LPS group (6.742 ± 0.128) g, PDTC group (7.137 ± 0.141) g; 1 week: control group (20.173 ± 3.982) g, LPS group (13.264 ± 2.581) g, PDTC group (17.863 ± 3.412) g]. In 1 week-old offspring of LPS group, the thoracic aortas exhibited lesions, including impaired endothelial cells, thickening and fibrous changes of intimae, and migration and proliferation of vascular smooth muscle cells; the number of gap junction was decreased versus control group and pathological changes were similar between PDTC group and LPS group. Cx43 protein expression in LPS group was obviously lower than in control group and which could be partly reversed in PDTC group. Expression of Cx43 mRNA was significantly lower in 1 day and 1 week offspring of LPS group compared to control group (P < 0.05), which could be reversed in PDTC group (P < 0.05) (1 day: control group 1.530 ± 0.296, LPS group 1.226 ± 0.209, PDTC group 1.619 ± 0.324; 1 week: control group 9.357 ± 1.917, LPS group 7.204 ± 1.165, PDTC group 9.271 ± 1.514).
Conclusion:
Our results indicate that maternal LPS exposure during pregnancy leads to vascular changes in neonatal offspring which might increase the susceptibility to adult hypertension.
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