NMDA-induced interleukin-1β expression is mediated by nuclear factor-kappa b p65 in the retina

摘要: Abstract Transcription factors of the nuclear factor-kappa B (NF-κB) p65/RelA may be involved in neuronal cell death. We examined involvement NF-κB p65 N-methyl- d -aspartate (NMDA)-induced upregulation interleukin (IL)-1β, a proinflammatory cytokine, and subsequent neurotoxicity rat retina. Immunohistochemistry showed that IL-1β is localized not only glial cells, but also neurons, especially retinal ganglion cells (RGCs) after intravitreal injection NMDA. Semi-quantitative real-time PCR NMDA induces an increase mRNA levels. Preinjection antisense oligodeoxynucleotide (AS ODN) ameliorated NMDA-induced expression. Western blot analysis elevated levels protein 12 h this elevation was significantly inhibited by AS ODN. Neurotracer labeling inhibition ODN or siRNA exerted protective effect against RGC loss. had on number NMDA-treated eyes. Penetration to layer inner confirmed with rhodamine Cy3. These results suggest participate induction expression death use viable neuroprotective strategy for survival.