earticle

영어

Amyloid β peptide (Aβ) still best known as a molecule to cause Alzheimer's disease (AD). AD is characterized by the accumulation and deposition of Aβ within the brain, leading to neuronal cell loss and perturbation of synaptic function by causing free radical formation, inflammation and apoptosis. We investigated the inflammatory action of Aβ on two types of brain cells, neuronal cells (SH-SY5Y) and neuroglia cells (C6), and its mechanism. We measured the production of NO-iNOS, TNF-α, and ICAM-1 using RT-PCR and Western blot analysis less than the concentration of cytotoxic effects (> 70% survivability). Aβ had no effect on the production of NO and TNF-α, but significantly increases of iNOS and ICAM-1. Based on this, we suggest that the inflammatory effect of Aβ results from the action of ICAM-1 in neuronal cells, rather than the release of inflammatory mediators such as NO and TNF-α in neuroglia cells. In addition, we confirmed whether p53 was related to the action of Aβ by using SH-SY5Y (p53-/-) dominant cells. Neither the expression of p53 nor the cytotoxicity of SH-SY5Y (p53-/-) cells were directly affected by Aβ. However, ICAM-1 was not expressed in SH-SY5Y (p53-/-) cells. This means that p53- independent pathway exists in the expression of ICAM-1 by Aβ while p53 plays a role as an on-and-off switch.