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

Abstract

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, and tauopathy are associated factors of AD. Sodium butyrate (NaB) is an HDAC inhibitor profoundly found to be neuroprotective. We have investigated the neuroprotective effects of NaB in SH-SY5Y cells stimulated with TNF-α/Aβ in SH-SY5Y cells and LPS-induced BV-2 cells. The cell viability and NO production were also investigated by MTT and Griess reagent assay. The expressions of APP/BACE, Aβ, and tau phosphorylation and the apoptotic regulators, including P-53, and caspase-1 were analysed by western blot analysis. Our findings exerted that NaB ameliorated cell death and inhibited NO production in Aβ-induced SH-SY5Y cells and LPS in BV-2 cells. NaB notably decreased the expression of tau hyperphosphorylation in TNF-α-stimulated SH-SY5Y and LPS-induced BV-2 cells. NaB remarkably attenuated APP/BACE and Aβ expressions in TNF-α-induced SH-SY5Y cells. Cell viability was restored by NaB and downregulated apoptotic proteins p-53, caspase-1 level in aggregated Aβ-induced SH-SY5Y cells. NaB increased Nrf-2/HO-1 expressions and substantially reversed the reactive oxygen species in Aβ-induced SH-SY5Y cells. Altogether, our results suggest that NaB could be a potential therapeutic agent against AD.