Turkish journal of biology = Turk biyoloji dergisi · 2026
Profiling arbutin as a potent cholinesterase and GSK-3β inhibitor and evaluating its cytotoxicity in SH-SY5Y cells for Alzheimer's disease therapy.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tarbiat Shirin, Bal Tuğba, Gülmez Deniz
Аннотация
BACKGROUND/AIM: Alzheimer's disease (AD) is a neurodegenerative disorder linked to cognitive decline and memory loss, marked by hyperphosphorylated tau tangles and decreased acetylcholine levels, which are affected by acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activity. Glycogen synthase kinase-3 beta (GSK-3β) also plays a role in AD through abnormal activation. In this study, the potential of β-arbutin to inhibit cholinesterases and GSK-3β was investigated, utilizing in vitro assays, cytotoxicity analysis, and molecular docking simulations to explore its therapeutic implications.
MATERIALS AND METHODS: Ellman's technique was used to test the inhibitory effects of arbutin on cholinesterase enzymes. An ATP-Glo luminescent assay kit was used to evaluate the inhibitory effects and inhibition kinetics of arbutin on GSK-3β. A Cell Titer-Glo 2.0 assay kit was used to assess the cytotoxicity of arbutin in SH-SY5Y cells.
RESULTS: β-Arbutin exhibited significant inhibitory effects on AChE, BuChE, and GSK-3β, with IC50 values of 0.6, 4, and 1.23 μM, respectively. The inhibition kinetics of GSK-3β with respect to ATP was competitive but with respect to the substrate (GS-2) was noncompetitive. We further found that β-arbutin, when applied alone to SH-SY5Y cells, does not affect cell viability and can ensure the sustainability of cell viability and health. Docking scores were -7.980, -6.726, and -6.115 kcal/mol for GSK-3β, AChE, and BuChE, respectively.
CONCLUSION: Our research demonstrates that arbutin is a modulator of cholinesterase and GSK-3β and may be beneficial as a multitarget-directed therapeutic natural compound for AD.
MATERIALS AND METHODS: Ellman's technique was used to test the inhibitory effects of arbutin on cholinesterase enzymes. An ATP-Glo luminescent assay kit was used to evaluate the inhibitory effects and inhibition kinetics of arbutin on GSK-3β. A Cell Titer-Glo 2.0 assay kit was used to assess the cytotoxicity of arbutin in SH-SY5Y cells.
RESULTS: β-Arbutin exhibited significant inhibitory effects on AChE, BuChE, and GSK-3β, with IC50 values of 0.6, 4, and 1.23 μM, respectively. The inhibition kinetics of GSK-3β with respect to ATP was competitive but with respect to the substrate (GS-2) was noncompetitive. We further found that β-arbutin, when applied alone to SH-SY5Y cells, does not affect cell viability and can ensure the sustainability of cell viability and health. Docking scores were -7.980, -6.726, and -6.115 kcal/mol for GSK-3β, AChE, and BuChE, respectively.
CONCLUSION: Our research demonstrates that arbutin is a modulator of cholinesterase and GSK-3β and may be beneficial as a multitarget-directed therapeutic natural compound for AD.