Purine nucleosides: endogenous neuroprotectants in hypoxic brain.

摘要: Abstract Even a short blockade of oxygen flow in brain may lead to the inhibition oxidative phosphorylation and depletion cellular ATP, which results profound deficiencies function. Following ischemia, dying, injured, hypoxic cells release soluble purine-nucleotide -nucleoside pools. Growing evidence suggests that purine nucleosides might act as trophic factors CNS PNS. In addition equilibrative nucleoside transporters (ENTs) regulating concentrations intra- extracellularly, specific extracellular receptor subtypes for these compounds are expressed on neurons, glia, endothelial cells, mediating stunningly diverse effects. Such effects range from induction cell differentiation, apoptosis, mitogenesis, morphogenetic changes, stimulation synthesis and/or cytokines neurotrophic under both physiological pathological conditions. Multiple signaling pathways regulate critical balance between death survival hypoxia–ischemia. A convergent pathway regulation multiple modalities involved O2 sensing is mitogen activated protein kinase (p42/44 MAPK) or (ERK1/2 signal-regulated kinases) terminating variety transcription factors, example, hypoxia-inducible factor 1α. this review, coherence nucleoside-related MAPK activation endogenous neuroprotective nervous system's development neuroplasticity stress will be discussed.