ArticleFrontiers in pediatrics2022
Multi-Hit White Matter Injury-Induced Cerebral Palsy Model Established by Perinatal Lipopolysaccharide Injection.
Article in Frontiers in pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- CD11c + microglia: From basic research to clinical application.Neural regeneration research · 2026Article
- IMR-1 ameliorates perinatal LPS-induced brain injury by promoting the conversion of glial cells into neurons.Journal of molecular histology · 2026Article
- Intracranial LPS injection induces cerebral palsy-like motor and behavioral deficits in immunodeficient mice.Scientific reports · 2026Article
- Chrono-combined aerobic-resistance exercises as therapeutic approach to reverse neurodegeneration in rat model: a detailed protocol.Frontiers in aging neuroscience · 2026Article
- Combined Maternal Immune Activation and Prenatal Intermittent Hypoxic Stress Lead to Developmental Motor Deficits in Rats: a Two-hit Animal Model for Cerebral Palsy Across Different Age Trajectories.Molecular neurobiology · 2025Article
- Wnt1 oversees microglial activation by the Wnt/LRP5/6 receptor signaling pathway during lipopolysaccharide-mediated toxicity.Molecular biology reports · 2025Article
- Prenatal inflammation exacerbates hyperoxia-induced neonatal brain injury.Journal of neuroinflammation · 2025Article
- Oral ellagic acid attenuated LPS-induced neuroinflammation in rat brain: MEK1 interaction and M2 microglial polarization.Experimental biology and medicine (Maywood, N.J.) · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral palsy (CP) is a group of permanent, but not unchanging, disorders of movement and/or posture and motor function. Since the major brain injury associated with CP is white matter injury (WMI), especially, in preterm infants, we established a "multi-hit" rat model to mimic human WMI in symptomatology and at a histological level. In our WMI model, pups suffering from limb paresis, incoordination, and direction difficulties fit the performance of CP. Histologically, they present with fewer neural cells, inordinate fibers, and more inflammatory cell infiltration, compared to the control group. From the electron microscopy results, we spotted neuronal apoptosis, glial activation, and myelination delay. Besides, the abundant appearance of IBA1-labeled microglia also implied that microglia play a role during neuronal cell injury. After activation, microglia shift between the pro-inflammatory M1 type and the anti-inflammatory M2 type. The results showed that LPS/infection stimulated IBA1 + (marked activated microglia) expression, downregulated CD11c + (marked M1 phenotype), and upregulated Arg 1 + (marked M2 phenotype) protein expression. It indicated an M1 to M2 transition after multiple infections. In summary, we established a "multi-hit" WMI-induced CP rat model and demonstrated that the microglial activation correlates tightly with CP formation, which may become a potential target for future studies.
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