ArticleScientific reports2016
N-acetylcysteine attenuates lipopolysaccharide-induced impairment in lamination of Ctip2-and Tbr1- expressing cortical neurons in the developing rat fetal brain.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Pathophysiological associations between maternal immune activation and neurodevelopmental disorders in offspring: a comprehensive review.Frontiers in endocrinology · 2025Review
- Enhancing acute inflammatory and sepsis treatment: superiority of membrane receptor blockade.Frontiers in immunology · 2024Review
- Pannexin-1 opening in neuronal edema causes cell death but also leads to protection via increased microglia contacts.Cell reports · 2023Article
- The impact of maternal immune activation on embryonic brain development.Frontiers in neuroscience · 2023Review
- TNFα-Induced Oxidative Stress and Mitochondrial Dysfunction Alter Hypothalamic Neurogenesis and Promote Appetite Versus Satiety Neuropeptide Expression in Mice.Brain sciences · 2022Article
- Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury.International journal of molecular sciences · 2021Article
- N-acetylcysteine inhibits bacterial lipopeptide-mediated neutrophil transmigration through the choroid plexus in the developing brain.Acta neuropathologica communications · 2020Article
- QUEST MRI assessment of fetal brain oxidative stress in utero.NeuroImage · 2019Article
- ATM is activated by ATP depletion and modulates mitochondrial function through NRF1.The Journal of cell biology · 2019Article
- Article
- Prenatal influenza vaccination rescues impairments of social behavior and lamination in a mouse model of autism.Journal of neuroinflammation · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress and inflammatory insults are the major instigating events of bacterial intrauterine infection that lead to fetal brain injury. The purpose of this study is to investigate the remedial effects of N-acetyl-cysteine (NAC) for inflammation-caused deficits in brain development. We found that lipopolysaccharide (LPS) induced reactive oxygen species (ROS) production by RAW264.7 cells. Macrophage-conditioned medium caused noticeable cortical cell damage, specifically in cortical neurons. LPS at 25 μg/kg caused more than 75% fetal loss in rats. An increase in fetal cortical thickness was noted in the LPS-treated group. In the enlarged fetal cortex, laminar positioning of the early born cortical cells expressing Tbr1 and Ctip2 was disrupted, with a scattered distribution. The effect was similar, but minor, in later born Satb2-expressing cortical cells. NAC protected against LPS-induced neuron toxicity in vitro and counteracted pregnancy loss and alterations in thickness and lamination of the neocortex in vivo. Fetal loss and abnormal fetal brain development were due to LPS-induced ROS production. NAC is an effective protective agent against LPS-induced damage. This finding highlights the key therapeutic impact of NAC in LPS-caused abnormal neuronal laminar distribution during brain development.
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