In vitro neuroprotective effects of allicin on Alzheimer’s disease model of neuroblastoma cell line

Ufuk Okkay; Irmak Ferah Okkay

doi:10.28982/josam.1068336

Authors

Ufuk Okkay https://orcid.org/0000-0002-2871-0712
Irmak Ferah Okkay Atatürk Üniversitesi https://orcid.org/0000-0001-8836-9547

DOI:

https://doi.org/10.28982/josam.1068336

Keywords:

Allicin, Alzheimer’s disease, Antioxidant, Apoptosis, SH-SY5Y cell line

Abstract

Background/Aim: Alzheimer's disease is a progressive disorder that causes atrophy and neuronal death in the brain. Currently, there is not any effective therapy for Alzheimer's disease. The current research was designed to investigate the beneficial effects of allicin on Alzheimer’s disease in SHSY-5Y cells in vitro and elucidating the neuroprotective mechanism of allicin. Methods: Human neuroblastoma cell line (SH-SY5Y) was differentiated with retinoic acid to conduct the in vitro Alzheimer’s Disease model. Amyloid β1-42 protein was applied to the cells for 24 hours (2.5 µM) to induce cytotoxicity. Allicin was applied to the cell cultures in a wide spectrum dose (10 μM, 50 μM, 100 μM) to investigate neuroprotective effect against amyloid β for 24 hours. MTT and LDH analyses were performed to assess the cell viability. MDA and ROS concentrations and SOD activity were analyzed to determine the oxidative stress. Moreover, the effects of allicin on the caspase-3 expression in amyloid β induced neurotoxicity were determined by the RT-PCR analysis. Results: Amyloid β markedly decreased cell viability of SH-SY5Y in MTT analysis and elevated LDH levels. In contrast, in MTT analysis, the allicin markedly increased cell viability, indicating that allicin induces cell proliferation. Moreover, in LDH analysis, allicin treatment markedly decreased LDH release. Exposure to amyloid β markedly increased MDA and ROS levels, in comparison with the control. Moreover, amyloid β decreased activity of SOD in SH-SY5Y cells. Allicin markedly balanced out the amyloid β-induced MDA and ROS generation. In the same pathway, allicin increased activity of SOD in amyloid β -exposed SH-SY5Y cells. The caspase 3 expression was increased in amyloid β group in comparison to the control group and allicin markedly lowered the expression of caspase-3 levels. Conclusion: The beneficial effects of allicin on amyloid β -induced neurotoxicity on SH-SY5Y cells were reported for the first time in terms of cell viability, oxidative stress and apoptosis.

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