The Potential Protective Effect of Curcumin on Amyloid-β-42 Induced Cytotoxicity in HT-22 Cells

Background. We aimed to investigate the effect and mechanism of curcumin (CUR) in Alzheimer's disease (AD). Methods. Mouse hippocampal neuronal cell line HT-22 was treated with A beta 1-42 and/or CUR, and then cell viability was evaluated by cell counting kit 8, Beclin-l level was detected using western blotting, and the formation of autophagosomes was observed by transmission electron microscopy (TEM). Furthermore, transcriptome sequencing and analysis were performed in cells with A beta 1-42 alone or A beta 1-42 + CUR. Results. A beta 1-42 treatment significantly inhibited cell viability compared with untreated cells (P < 0.01). After treatment for 48 h, CUR remarkably promoted cell viability compared with cell treated with A beta 1-42 alone (P < 0.01). Compared with cells treated with A beta 1-42 alone, the expression of Beclin-1 was slightly reduced in cells with combined treatment of A beta 1-42 with CUR (P < 0.05). Consistently, TEM results showed that CUR inhibited the formation of autophagosomes in cells treated with A beta 1-42. Furthermore, the protein-protein interaction network showed five key genes, including MYC, Cdh1, Acaca, Egr1, and CCnd1, likely involved in CUR effects. Conclusions. CUR might have a potential neuroprotective effect by promoting cell viability in AD, which might be associated with cell autophagy. Furthermore, MYC, Cdh1, and Acaca might be involved in the progression of AD.