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Abstract

Cerebral palsy is the most common cause of disability in children worldwide, estimated prevalence of 1.5–4 per 1000 children; the higher prevalence in low-resource populations (up to 10 per 1000 children). Brain-derived neurotrophic factor (BDNF) is potent modulator of many neuronal functions that protect the newborn or developing brain from ischemic injury. The expression of GluN3A, which plays a neuroprotective role, is rapidly induced during cerebral ischemia and hypoxia. This study assessed the effect of piracetam administration on BDNF and GluN3A levels in the brain tissue to determine its potential to prevent cerebral palsy. In this experimental study with a post-test-only control group design, a rat model of cerebral palsy was established by injecting pregnant rats with LPS on gestation days 15, 17, and 19; piracetam was administered orally on day 10.5. BDNF and GluN3A protein levels and mRNA expression in the foetal brain tissue of 36 subjects were evaluated with enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR). BDNF and GluN3A protein levels in the foetal brain differed significantly between the control and treatment groups (p < 0.05). A decrease in the mRNA and protein levels of BDNF and GluN3A was observed in all treatment groups, but the statistical analysis of RT-PCR did not reveal significant differences between the control and treatment groups (p > 0.05). These results indicate that piracetam can prevent cerebral palsy in a foetal rat model established via prenatal LPS injection, as assessed by the protein expression of BDNF and GluN3A mRNA.

Keywords

BDNF, Cerebral palsy, GluN3A, piracetam, rats.

Article Type

Supplemental Issue

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