Inhibition of CCAAT/enhancer binding protein δ expression by chrysin in microglial cells results in anti‐inflammatory and neuroprotective effects

摘要: J. Neurochem. (2010) 115, 526–536. Abstract The control of neuroinflammation is a potential target to be considered in the treatment neurodegenerative diseases. It therefore important find anti-inflammatory drugs and study new targets that inhibit neuroinflammation. We designed an experimental model vitro neuroprotective effects flavonoid chrysin involvement nuclear factor-κB p65 CCAAT/enhancer binding proteins (C/EBPs) β δ transcription factors its mechanism action. used primary cultures mouse embryonic cortical neurons BV2 (murine microglial cell line) or microglia. induced neuronal death neuronal-BV2/microglial co-cultures using lipopolysaccharide Escherichia coli interferon-γ. Chrysin pre-treatment inhibited nitric oxide tumor necrosis factor-α production, as well inducible synthase expression E. interferon-γ-treated cells, but did not affect cyclooxygenase-2 expression. also protected against neurotoxicity by reactive cells. These were associated decrease C/EBPδ protein level, mRNA expression, DNA-binding activity, with no effect on C/EBPβ levels pointing out possible mediator effects. Consequently, act processes.