Figure 7
From: Chronic ethanol increases systemic TLR3 agonist-induced neuroinflammation and neurodegeneration
Superoxide formation and oxidative stress in brain. Mice were injected with hydroethidine (dihydroethidium, 10 mg/kg, i.p.) 2.5 hours after poly I:C treatment and brains harvested 30 minutes later, frozen and sectioned (15 μm thickness) as described in the methods. The oxidation product, ethidium, is formed from dihydroethidium by superoxide resulting in ethidium accumulation within cells producing superoxide. Ethidium is detected as red nuclei by fluorescence microscopy. The level of fluorescence intensity of ethidium-positive cells was quantified by BioQuant image analysis software. (A) Quantitation of ethidium fluorescence indicates ethanol, poly I:C and ethanol + poly I:C treatment significantly increases O2 - and O2 --derived oxidant production in cortex. (B) Representative images of ethidium fluorescence. Ethanol and poly I:C alone increased O2 - and O2 --derived oxidant production compared with vehicle control. Ethanol pretreatment significantly potentiated poly I:C-induced O2 - and O2 --derived oxidant production. **P <0.01, compared with vehicle control group. ## P <0.01 compared with poly I:C group. Scale bar, 200 μm.