Abstract
Ethanol causes changes in the toll-like receptor (TLR) system in the brain promoting activation of neuroinflammatory pathways. Alcohol consumption during pregnancy induces neuroinflammatory processes in the fetus, which can lead to the development of symptoms of fetal alcohol spectrum disorder (FASD). Modeling prenatal alcohol exposure in our experiment resulted in changes in the expression of TLR system genes (Tlr3, Tlr4, Hmgb1, Trif, cytokine genes) in the forebrain cortex of baby rats. The administration of rifampicin (from the first to the seventh day of neonatal development) normalized the altered expression level of the studied genes. This suggests that rifampicin may prevent the development of persistent neuroinflammatory phenomena in the forebrain cortex of baby rats.
Published Version
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