β-Amyloid and interleukin-1β induce persistent NF-κB activation in rat primary glial cells

• DOI: 10.3892/ijmm.16.3.449
• Publication Date: 2014-03-10T07:37:36Z
• Authors: Malin Samuelsson; Linda Fisher; Kerstin Iverfeldt
• Keywords: 0301 basic medicine; 03 medical and health sciences; 0302 clinical medicine

An increasing body of evidence suggests that β-amyloid (Aβ) and activated glial cells play a crucial part in the pathogenesis Alzheimer's disease (AD). Activated surrounding senile plaques, formed by Aβ peptides, have been proposed to promote neurodegeneration producing putatively toxic factors, including inflammatory cytokine interleukin-1β (IL-1β). Elevated levels both IL-1β nuclear factor κB (NF-κB), key transcription regulating wide variety genes, found brains AD patients. In this study, we investigated ability Aβ(25-35) peptide IL-1β, either alone or together, activating NF-κB cells. Mixed primary from rat were treated with and/or Aβ(25-35), binding activity was analyzed electophoretic mobility shift assay. We observed induction induced showed peak at 30 min, significantly declined after 2 h. The activation persisted 24 h even seemed increase Aβ(25-35). shown be dose-dependent. addition, potentiated effect dose-dependent manner when co-stimulating potentiating on IL-1β-induced h, did not differ over time. A possible explanation is are stimulated factors presence peptides negative feedback regulation no longer functional.