Neuronal death and survival in two models of hypoxic-ischemic brain damage.

摘要: Abstract Two unilateral hypoxic-ischemia (HI) models (moderate and severe) in immature rat brain have been used to investigate the role of various transcription factors related proteins delayed neuronal death survival. The moderate HI model results an apoptotic-like selectively vulnerable regions while more severe injury consistently produces widespread necrosis resulting infarction, with some resistant cell populations showing evidence apoptotic type death. In susceptible undergoing there was not only a prolonged induction immediate early genes, c- jun , fos nur77 but also possible target genes amyloid precursor protein (APP 751 ) CPP32. contrast, increased levels BDNF, phosphorylated CREB PGHS-2 were found cells insult suggesting that these either alone or combination may be importance process neuroprotection. An additional feature both insults rapid activation and/or proliferation glial (microglia astrocytes) around site damage. response following associated upregulation CCAAT-enhancer binding α only) NFκB factors.