Inhibition of NF-κB might enhance the protective role of roflupram on SH-SY5Y cells under amyloid β stimulation via PI3K/AKT/mTOR signaling pathway.

NF-kappa B; AMYLOID; LABORATORY mice; DISEASE progression; NUCLEAR models; TRICARBOXYLIC acids

Alzheimer disease (AD) is a progressive neurodegenerative disease and mostly endanger the health of people older than 65 years. Accumulation of beta amyloid protein (Aβ) is the main characteristic of AD. Roflupram (ROF) could improve the behavior of AD in a mouse model. In this study, we first detected the increased concentration of molecules related to inflammatory response in serum sample of patients with AD. Next, a cell model of nuclear factor kappa B (NF-κB) inhibition and NF-κB overexpression was established in SH-SY5Y cells, Aβ was used to simulate the toxicity to cells. ROF treatment decreased expression of apoptosis-related molecules via inhibition of PI3K/AKT/mTOR signaling pathway, decreased expression of pro-inflammatory factors, and increased expression of key enzymes in the tricarboxylic acid (TCA) cycle was observed in SH-SY5Y cells after ROF treatment. Inhibition of NF-κB could enlarge these trends whereas overexpression of NF-κB could reduce these trends. [ABSTRACT FROM AUTHOR]

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