کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3070991 | 1580752 | 2006 | 13 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Anti-inflammatory treatment in oxygen–glucose-deprived hippocampal slice cultures is neuroprotective and associated with reduced cell proliferation and intact neurogenesis Anti-inflammatory treatment in oxygen–glucose-deprived hippocampal slice cultures is neuroprotective and associated with reduced cell proliferation and intact neurogenesis](/preview/png/3070991.png)
Increased neurogenesis in response to brain injury is considered a mechanism of regeneration after neuronal loss. Using organotypic hippocampal cultures (OHC), we investigated the interplay between neuronal damage (propidium iodide uptake), microglia activation (OX-42 immunohistochemistry), cell proliferation (bromodeoxyuridine incorporation), and neurogenesis (double labeling of bromodeoxyuridine with doublecortin or β-III tubulin) after oxygen–glucose deprivation (OGD). We observed that microglia activation and upregulation of pro-inflammatory cytokines mRNA preceded neuronal loss and was followed by increased cell proliferation. Neurogenesis was inhibited 3 days after OGD in both neurogenic zones of the slice, the dentate gyrus and the posterior periventricle (pPV). After 6 days, neurogenesis was restored and significantly increased in the pPV. Indomethacin or minocycline reduced the OGD-induced damage, proliferation, and increase of microglia. Both agents did not interfere with OGD-induced pPV neurogenesis. Our study shows for the first time that neuroprotection against OGD-induced damage in OHC by anti-inflammatory treatment is associated with intact neurogenesis.
Journal: Neurobiology of Disease - Volume 23, Issue 2, August 2006, Pages 247–259