Abstract—The main purpose of this study was to evaluate whether donepezil and Low-Level Light Therapy (LLLT) shown to play neuroprotective effects by stimulating mitochondrial activity in the amyloid-beta 1-42 (Aβ1-42) -induced neuronal toxicity model of Alzheimer’s Disease (AD). This result indicates that the Aβ1-42 accumulation in neuronal cells is related to the mitochondrial dysfunction and induced-neuronal cell death. While donepezil and Low-Level Light Therapy (LLLT; 660 nm, 5mW/cm2, 3J/ cm2) can reverse this situation. Donepezil is therapeutic acetylcholinesterase inhibitor currently being used for the treatment of AD. SH-SY5Y cells were pre-treated by donepezil at a concentration of 1 µM showed a maximum of neuronal viability compared to control cells. However, at higher concentrations, the neuronal viability was diminished. LLLT is a noninvasive therapy which showed significant increasing of neuronal viability and afforded protection against Aβ1-42-induced toxicity. In addition, the combination treatment between 1 µM of donepezil pre-treatment and LLLT in SH-SY5Y cells induced by Aβ1-42 toxicity had increased cell viability. In aggregate, these results demonstrate that LLLT has probably contributed to alternative treatment in neurodegenerative disease. 

Index Terms—Alzheimer’s disease, Beta-Amyloid, low-level light therapy, donepezil hydrochloride

Cite:Siriluk Thammasart and Kwanchanok Viravaidya-Pasuwat, and Anak Khantachawana, "The Study of Protective Effects of Low-Level Light and Donepezil Against β-Amyloid-Induced Cytotoxicity in SH-SY5Y Cells," International Journal of Pharma Medicine and Biological Sciences, Vol. 8, No. 3, pp. 100-105, July 2019. doi: 10.18178/ijpmbs.8.3.100-105