Related Experiment Video
Updated: May 3, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Maternal exposure to advanced oxidation protein products induces neurodevelopmental abnormalities in the offspring of
Jiexing He1, Qian Chen1, Mingzheng Zhu1
1Department of Obstetrics & Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Insights
Preeclampsia (PE) exposure in pregnant mice led to offspring with learning and memory deficits. Oxidative stress and inflammation in the placenta appear to drive these neurodevelopmental abnormalities.
Area of Science:
- Reproductive biology
- Neuroscience
- Toxicology
Background:
- Preeclampsia (PE) causes maternal organ damage and long-term neurodevelopmental issues in offspring.
- Advanced oxidation protein products (AOPPs) are linked to PE pathogenesis via oxidative stress and inflammation.
- The impact of AOPPs-induced placental dysfunction on offspring neurodevelopment is not fully understood.
Purpose of the Study:
- To investigate whether prenatal exposure to AOPPs-induced placental oxidative stress affects offspring neurodevelopment.
- To elucidate the underlying mechanisms of AOPPs-induced neurodevelopmental abnormalities in offspring.
Main Methods:
- Pregnant mice were injected with AOPPs and AOPPs-induced small extracellular vesicles (sEVs) to induce PE-like symptoms.
- Offspring behavior was assessed for learning and memory impairments.
- Placental and hippocampal tissues underwent transcriptome sequencing.
Main Results:
- AOPP-injected mice exhibited PE-like symptoms, including elevated blood pressure and reduced fetal weight.
- Offspring exposed prenatally to AOPPs showed significant impairments in learning and memory.
- Transcriptome analysis indicated inflammation and immune responses play a key role.
Conclusions:
- Prenatal exposure to AOPPs-induced placental oxidative stress leads to neurodevelopmental and cognitive deficits in offspring.
- Inflammation and immune responses are critical mechanisms underlying these adverse effects.
- Findings offer insights for preventing and treating neurodevelopmental issues in offspring affected by PE.
Abstract:
Preeclampsia (PE) not only causes multi-organ damage to the mother but also exerts long-term effects on the development of the offspring. Prenatal exposure to PE has been demonstrated to result in deleterious neurodevelopment and behavioral abnormalities in the offspring. Our prior research has evidenced that advanced oxidation protein products (AOPPs), both the biomarker and promoter of oxidative stress, contribute to the pathogenesis of preeclampsia by inducing trophoblast dysfunction and systemic inflammation. However, it remains unclear whether offspring mice exposed to placental oxidative stress and dysfunction induced by AOPPs will exhibit abnormal neurodevelopment and the underlying mechanisms involved. In this study, we found pregnant mice injected with AOPPs and AOPPs-induced sEVs exhibited PE-like symptoms with elevated blood pressure and reduced fetal weight. Furthermore, behavioral detection showed that male and female adult offspring mice exposed to AOPPs prenatally displayed impairments in learning and memory. Placental and hippocampal transcriptome sequencing revealed that inflammation and immune response may play a pivotal role in this process. Our study provides valuable insights into the pathogenesis of adverse neurodevelopment and cognitive dysfunction in offspring exposed to placental oxidative stress induced by AOPPs and the search for effective preventive and therapeutic measures.
