Sodium butyrate alleviates potential Alzheimer’s disease in vitro by suppressing Aβ and tau activation and ameliorates Aβ-induced toxicity

The number of Alzheimer’s disease (AD) affected patients is increasing without any effective cure and the etiology remains to be understood. Inflammations, oxidative stress, Aβ, tauopathy are associated factors AD. Sodium butyrate (NaB) an HDAC inhibitor profoundly found neuroprotective. We have investigated neuroprotective effects NaB in SH-SY5Y cells stimulated with TNF-α/Aβ LPS-induced BV-2 cells. cell viability NO production were also by MTT Griess reagent assay. expressions APP/BACE, tau phosphorylation apoptotic regulators, including P-53, caspase-1 analysed western blot analysis. Our findings exerted that ameliorated death inhibited Aβ-induced LPS notably decreased expression hyperphosphorylation TNF-α-stimulated remarkably attenuated APP/BACE Aβ TNF-α-induced Cell was restored downregulated proteins p-53, level aggregated increased Nrf-2/HO-1 substantially reversed reactive oxygen species Altogether, our results suggest could a potential therapeutic agent against