Small molecule compounds alleviate anisomycin-induced oxidative stress injury in SH-SY5Y cells via downregulation of p66shc and Aβ1–42 expression

摘要: Oxidative stress and ageing are important factors contributing to the pathogenesis of Alzheimer's disease (AD), which is associated with neuronal damage β-amyloid (Aβ) deposition. The p66shc adaptor protein for regulation oxidative ageing. In present study, SH-SY5Y human neuroblastoma cells were treated anisomycin in order establish a cell model stress-induced damage. results from quantitative polymerase chain reaction, enzyme-linked immunosorbent assay western blotting demonstrated that was able stimulate secretion Aβ1-42 upregulate expression levels p66shc, concomitant cells. addition, protective effects various small molecule compounds antioxidant properties against evaluated. Notably, treatment gallic acid significant downregulation levels, reduced anisomycin-induced Aβ1-42, increased superoxide dismutase activity acetylcholine levels. study suggested promote by inducing neurons increasing this may be attenuated acid. Therefore, similar considered alleviation injury patients AD.