作者: E. Viggiano , D. Ferrara , G. Izzo , A. Viggiano , S. Minucci
DOI: 10.1016/J.NEUROSCIENCE.2008.01.037
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摘要: Abstract The mechanisms of tolerance to subsequent episodes ischemia induced by cortical spreading depression (CSD) are not clear. effects CSD on the expression inducible nitric oxide synthase (iNOS), hypoxia factor-1α (HIF-1α), and lactate dehydrogenase-A (LDH-A) were evaluated in present experiment. Unilateral was Sprague-Dawley rats application KCl right cortex mRNA levels iNOS, HIF-1α, LDH-A at 15 min, 2 h, 4 6 h or 24 after CSD. RT-PCR analysis showed: 1) an increase iNOS h; 2) HIF-1α 3) h. In situ hybridization with specific digoxigenin-labeled oligonucleotides revealed that increased min–2 for 2–4 HIF-1 Immunohistochemistry increased, respectively, These data suggest promotes nervous cells giving a neuroprotective effect.