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Background This study aimed to establish an in vitromodel of Alzheimer’s Disease (AD) to investigate the neuroprotective activities of allyl isothiocyanate (AITC) and sulforaphane (SFN).Materials and Methods Human neuroblastoma cell lines (SKNAS) were used for the in vitromodel of AD after amyloid-β25−35(Aβ25–35) treatment. Cytotoxicity analysis was performed using the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay. Indirect immunocytochemical methods were used to assess the tau protein, alpha-synuclein (α-synuclein), and β-amyloid distribution in the in vitromodel of AD and SKNAS cells.Results An in vitroAD model was induced by treatment of SKNAS cells with 1 µM of Aβ25–35for 48 h. AITC and SFN were applied for 48 h, and the optimal concentrations were determined as 50 µM AITC and 15 µM SFN. Reduced tau immunoreactivity was shown after AITC and SFN administration in SKNAS cells and in vitromodels, demonstrating that AITC and SFN prevented amyloid plaque production in the in vitroAD model control group by reducing the β-amyloid level, α-synuclein levels were similar in control and in vitroAD model cells. Reduced α-synuclein levels were observed after SFN treatment in the AD model cells and AITC treatment in the control cells.Conclusion It could be concluded that AITC and SFN are potential components as neuroprotective agents against AD.

AbstractObjective:Hesperidin and naringin are flavonoids that are found in citrus fruits. Our aim was to create an in vitromodel of Alzheimer’s disease (AD) and to evaluate the neuroprotective effects of hesperidin and naringin in SK-N-AS and AD model cells.Methods:Aβ25-35was used to create an AD model in SK-N-AS cells. The cytotoxicity of hesperidin and naringin was evaluated using MTT. β-amyloid, tau and α-synuclein distributions were analyzed using indirect immunoperoxidase staining to investigate the neuroprotective effects of hesperidin and naringin.Results:The AD model was created by 1 µM of Aβ25-35for 48 hours after ThT staining. The intensity of β-amyloid was reduced through both hesperidin and naringin treatment in AD model cells. Both flavonoids significantly decreased the intensity of α-synuclein in SK-N-AS and AD model cells.Conclusions:Hesperidin and naringin can be potentially used as neuroprotective agents. Naringin may be more effective than hesperidin in the accumulation of β-amyloid and tau proteins.

Background: Quercetin is a flavonol from the flavonoid group of polyphenols, which positively affects human health due to its anti-cancer, anti-inflammatory, anti-microbial and cardioprotective effects. The effects of phenolic compounds, including quercetin, on programmed cell death and cellular senescence, have been the subject of research in recent years. Objective: In this study, we aimed to investigate the effects of quercetin on cell viability, apoptosis and cellular senescence in primary (Colo-320) and metastatic (Colo-741) colon adenocarcinoma cell lines. Methods: Cytotoxicity was analyzed via MTT assay in Colo-320 and Colo-741 cell lines. After quercetin treatment, cell ularsenescence and apoptosis were evaluated by TUNEL staining, X-Gal staining and indirect peroxidase technique for immunocytochemical analysis of related proteins such as Bax, Bcl-2, caspase-3, Hsp27, Lamin B1, p16, cyclin B1. Results: The effective dose for inhibition of cell growth in both cell lines was determined to be 25μg/ml quercetin for 48 hours. Increased Baximmunoreactivityfollowingquercetin treatment was significant in both Colo-320 and Colo-741 cell lines, but decreased Bcl-2 immunoreactivitywas significant only in theColo-320 primary cell line. In addition, after quercetin administration, the number of TUNEL positive cells and, immunoreactivities for p16, Lamin B1 and cyclin B1 in both Colo-320 and Colo-741 cells increased. Conclusion: Our results suggest that quercetin may only induce apoptosis in primary colon cancer cells. Furthermore, quercetin also triggered senescence in colon cancer cells, but some cells remained alive, suggesting that colon cancer cells might have escaped from senescence.