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In studies of neuroinflammation models (n = 7), both erinacine A and HEME protected N2a neuronal cells from lipopolysaccharide (LPS)-exposed BV-2 conditioned medium-induced cell death through the suppression of c-Jun N-terminal kinase (JNK) and nuclear factor kappa-light-chain-enhancer of activated B (NF-B) activation ( In primary cortical glia-neuron co-cultures, erinacine A improved neuronal and astrocyte survival and preserved astrocyte glutamate homeostasis in response to oxygen-glucose deprivation via the accumulation of glutamate transporter 1 protein levels ( tert -butylhydroperoxide-induced oxidative stress human neuroblastoma cell model ( In whole-brain mixed glia co-cultures following LPS insult, erinacine C induced the expression of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), which was correlated with increased protein expression of BDNF and other antioxidant enzymes ( Neurotrophic effects Under normal conditions, acute treatments with erinacine A, erinacine C, or erinacine S induced neurite-outgrowth of PC12 neurons in the presence of NGF, and also induced NGF release from astrocytic cells in 1321N1 cell models ( Summary In vitro studies on H

Burdon, C.A., M.W