作者: Dasa Cizkova , Jason B. Carmel , Kenji Yamamoto , Osamu Kakinohana , Dongming Sun
DOI: 10.1016/J.EXPNEUROL.2003.09.020
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摘要: Abstract Induction of heat shock protein (HSP72) has been implicated in the development ischemic tolerance several tissue organs including brain and spinal cord. In present study, using an aortic balloon occlusion model rats, we characterized effect transient noninjurious (3 or 6 min) injurious intervals (10 ischemia followed by 4–72 h reflow on expression HSP72 GFAP protein. a separate group animals, preconditioning recovery function after interval was studied. After 3 min ischemia, there modest increase immunoreactivity dorsal horn neurons at 12 reperfusion. more robust wide spread both ventral detected. The peak seen 24 ischemia. At same time point, significant measured with Western blots corresponded morphologically presence activated astrocytes segments that had treated similarly. 10 reflow, neuronal perinecrotic regions seen. Behaviorally, led to biphasic (the first 30 second preconditioning) expressed as significantly better motor exposure 10-min preconditioning, then 3-min These data indicate represents threshold for induction, however, longer sublethal (6 is required potent induction. More neurological protection, also indicates interneurons may represent important variable modulating observed during this frame.