Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat-6

layers of hippocampus (B), indicating severe neural injury. OX-42 immunoreactivity showed CD11b – expressing cells at the cortical lesion site (C). Hippocampal OX-42 localized to the molecular layer of dentate gyrus and was evident in hippocampal regions seated ventral to CA1, but was not present in the pyramidal cell layers (D). Scale bars = 100 μm.<p><b>Copyright information:</b></p><p>Taken from "Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat"</p><p>http://www.jneuroinflammation.com/content/5/1/34</p><p>Journal of Neuroinflammation 2008;5():34-34.</p><p>Published online 11 Aug 2008</p><p>PMCID:PMC2527306.</p><p></p

Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat-0

Cortex (B) compared to contralateral control (A). CD11b – expressing cells were abundant in corpus striatum of both hemispheres but showed distinct morphology (C,D). Cells in the ipsilateral striatum displayed the activated amoeboid phenotype (D) similar to those in ipsilateral cortex (E) when compared to the ramified morphology in the contralateral hemisphere (C) that is associated with a less activated state. Scale bars = 100 μm (A,B), 50 μm (C-E).<p><b>Copyright information:</b></p><p>Taken from "Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat"</p><p>http://www.jneuroinflammation.com/content/5/1/34</p><p>Journal of Neuroinflammation 2008;5():34-34.</p><p>Published online 11 Aug 2008</p><p>PMCID:PMC2527306.</p><p></p

Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat-1

layers of hippocampus (B), indicating severe neural injury. OX-42 immunoreactivity showed CD11b – expressing cells at the cortical lesion site (C). Hippocampal OX-42 localized to the molecular layer of dentate gyrus and was evident in hippocampal regions seated ventral to CA1, but was not present in the pyramidal cell layers (D). Scale bars = 100 μm.<p><b>Copyright information:</b></p><p>Taken from "Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat"</p><p>http://www.jneuroinflammation.com/content/5/1/34</p><p>Journal of Neuroinflammation 2008;5():34-34.</p><p>Published online 11 Aug 2008</p><p>PMCID:PMC2527306.</p><p></p

Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat-4

Ult. Intense OX-42 immunoreactivity was evident throughout the ipsilateral cerebral cortex of animals treated with vehicle alone (B). Microglia/macrophage labeling was nearly abolished after treatment with minocycline (D) and was markedly reduced after treatment with AG3340 (F). OX-42 immunoreactivity in contralateral control regions was faint and diffuse by comparison (A,C,E). Scale bars = 100 μm.<p><b>Copyright information:</b></p><p>Taken from "Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat"</p><p>http://www.jneuroinflammation.com/content/5/1/34</p><p>Journal of Neuroinflammation 2008;5():34-34.</p><p>Published online 11 Aug 2008</p><p>PMCID:PMC2527306.</p><p></p

Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat-3

Ult. Animals treated with vehicle alone showed robust Fluoro-Jade labeling in ipsilateral cortex and corpus striatum (B). Fluoro-Jade staining was nearly abolished after treatment with minocycline (D) and greatly reduced after treatment with AG3340 (F) relative to vehicle alone (B). No labeling was detected in contralateral control regions (A,C,E). Quantification showed a significant reduction after treatment with either minocycline or AG3340 (G) compared to treatment with vehicle alone. N = 5, * = p < 0.05. Scale bars = 100 μm.<p><b>Copyright information:</b></p><p>Taken from "Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat"</p><p>http://www.jneuroinflammation.com/content/5/1/34</p><p>Journal of Neuroinflammation 2008;5():34-34.</p><p>Published online 11 Aug 2008</p><p>PMCID:PMC2527306.</p><p></p

Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat-5

Cortex (B) compared to contralateral control (A). CD11b – expressing cells were abundant in corpus striatum of both hemispheres but showed distinct morphology (C,D). Cells in the ipsilateral striatum displayed the activated amoeboid phenotype (D) similar to those in ipsilateral cortex (E) when compared to the ramified morphology in the contralateral hemisphere (C) that is associated with a less activated state. Scale bars = 100 μm (A,B), 50 μm (C-E).<p><b>Copyright information:</b></p><p>Taken from "Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat"</p><p>http://www.jneuroinflammation.com/content/5/1/34</p><p>Journal of Neuroinflammation 2008;5():34-34.</p><p>Published online 11 Aug 2008</p><p>PMCID:PMC2527306.</p><p></p