Microglial-produced nitric oxide and reactive nitrogen oxides mediate neuronal cell death.

摘要: The role of inflammatory cytokines in the pathogenesis neurological diseases is not well understood. neurotoxic effects could be mediated by immunostimulation glial cells to produce toxic concentrations nitric oxide (NO) and reactive nitrogen oxides. Cultured microglia meningeal fibroblasts, but Type 1 astrocytes, were induced lipopolysaccharides synthesize NO oxides from L-arginine. In co-cultures immunostimulated cerebellar granule neurons, neurotoxicity was blocked an inhibitor synthase, NG-nitroarginine, oxyhemoglobin, which inactivates NO. Microglial-induced also partially attenuated N-methyl-D-aspartate (NMDA) receptor antagonists, MK-801 2-amino-5-phosphovalerate (APV). Superoxide dismutase, stabilizes through inactivation superoxide anion, augmented microglial-mediated either alone or combination with APV. Hence, mediate NO, oxides, anion NMDA-like substances. These findings suggest a novel for microglial-produced as agent neurodegenerative disease states.