Targeting Oxidative Stress Injury after Ischemic Stroke in Conscious Rats: Limited Benefits with Apocynin Highlight the Need to Incorporate Long Term Recovery
Figure 4
Immunohistochemical localization of activated microglia/macrophages (OX42) and concurrent superoxide generation (dihydroethidium) in stroke-affected brain following vehicle control ((a)–(c)) and apocynin treatments ((d)–(f)). Fluorescence micrographs of the ipsilateral cortex with superoxide sensitive dihydroethidium ((a), (d)), the microglia marker OX42 ((b), (e)) and merged images ((c, (f)). Arrows point to a typical activated microglia cell in the ischemic core from both treatment groups. Quantification of microglial specific superoxide release in the core infarct region detected in situ 3 days after stroke in the isilateral cortex (stroke affected; solid bars) compared with the contralateral cortex (nonaffected; open bar) in vehicle control and apocynin treated rats (g). Quantification of microglial 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 OX-42 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 < 0.01; ###P < 0.0001 versus vehicle-treated. Scale bar = 100 μm.
