Targeting Oxidative Stress Injury after Ischemic Stroke in Conscious Rats: Limited Benefits with Apocynin Highlight the Need to Incorporate Long Term Recovery
Figure 5
Immunohistochemical localization of neurons (NeuN) and concurrent superoxide generation (dihydroethidium) in stroke-affected brain following vehicle control ((a)–(c)) and apocynin ((d)–(f)) treatments. Fluorescence micrographs of the ipsilateral cortex with superoxide-sensitive DHE ((a), (d)), the neuronal antibody NeuN ((b), (e)), and merged images ((c), (f)). Arrows point to a typical neuron in the ischemic core. Quantification of neuronal specific superoxide release in the core infarct region detected in situ 3 days after stroke in the ipsilateral cortex (stroke affected; solid bars) compared with the contralateral cortex (nonaffected; open bar) following ischemic stroke in vehicle control; apocynin-treated rats; apocynin-treated rats coincubated in the presence of rotenone in situ (g). Quantification of neuronal specific superoxide release in the core infarct region in the ipsilateral striatum compared with the contralateral striatum in vehicle control and apocynin-treated rats (h). Relative fluorescence was quantified by tracing around cells double labelled with NeuN and analysed using ImageJ software. Data are presented as mean ± SEM (n = 11 apocynin treated; n = 9 vehicle treated). *P < 0.05, **P < 0.01, and ***P < 0.001 versus contralateral mirror image; †††P < 0.001 versus vehicle treated; #P < 0.01 versus apocynin-treated total ipsilateral fluorescence. Scale bar = 100 μm.
