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  • Attenuation and augmentation of ischaemia-related neuronal death by tumour necrosis factor-alpha in vitro.

Attenuation and augmentation of ischaemia-related neuronal death by tumour necrosis factor-alpha in vitro.

The European journal of neuroscience (2000-11-09)
G J Wilde, A K Pringle, L E Sundstrom, D A Mann, F Iannotti
ABSTRACT

Upregulation of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNF) occurs rapidly in the brain following ischaemia, although it is unclear whether this represents a neurotoxic or neuroprotective response. We have investigated whether TNF has different actions in the pre- and postischaemic periods in a tissue culture model of cerebral ischaemia. Organotypic hippocampal slice cultures were prepared from 8-10-day-old rats and maintained in vitro for 14 days. Neuronal damage was induced by either 1 h oxygen-glucose deprivation or 3 h exposure to NMDA or the superoxide generator duroquinone, and assessed after 24 h by propidium iodide fluorescence. TNF pretreatment was neuroprotective against both oxygen-glucose deprivation and duroquinone. This effect was associated with an activation of the transcription factor NFkappaB and upregulation of manganese superoxide dismutase, and was prevented by a free radical scavenger. When addition of TNF was delayed until the postinsult period, an exacerbation of neurotoxicity occurred, which was also prevented by a free radical scavenger. The actions of TNF are determined by whether TNF is present before or after an ischaemia-related insult. Both actions are mediated through the production of free radicals, and the response to TNF is determined by whether a cell is metabolically competent to respond by synthesis of antioxidant defences.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Duroquinone, 97%
Supelco
Duroquinone, Standard for quantitative NMR, TraceCERT®