Sodium butyrate alleviates potential Alzheimer's disease in vitro by suppressing A & beta; and tau activation and ameliorates A & beta;-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, A & beta;, 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-& alpha;/A & beta; 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, A & beta;, 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 A & beta;-induced SH-SY5Y cells and LPS in BV-2 cells. NaB notably decreased the expression of tau hyperphosphorylation in TNF-& alpha;-stimulated SH-SY5Y and LPS-induced BV-2 cells. NaB remarkably attenuated APP/BACE and A & beta; expressions in TNF-& alpha;-induced SH-SY5Y cells. Cell viability was restored by NaB and downregulated apoptotic proteins p-53, caspase-1 level in aggregated A & beta;-induced SH-SY5Y cells. NaB increased Nrf-2/HO-1 expressions and substantially reversed the reactive oxygen species in A & beta;-induced SH-SY5Y cells. Altogether, our results suggest that NaB could be a potential therapeutic agent against AD.

Automated summary

The number of Alzheimer's disease (AD) affected patients is increasing and effective cure is still unavailable. Inflammation, oxidative stress, Aβ, and tauopathy are associated factors of AD. Sodium butyrate (NaB), an HDAC inhibitor, has been found to be neuroprotective. This study investigated the neuroprotective effects of NaB in cells stimulated with TNF-α/Aβ and LPS. The results showed that NaB reduced cell death and NO production, decreased tau hyperphosphorylation and APP/BACE, Aβ expressions, restored cell viability, downregulated apoptotic proteins, increased Nrf-2/HO-1 expressions, and reversed reactive oxygen species. These findings suggest that NaB could potentially be a therapeutic agent against AD.