Abstract

Rhodiola rosea L. (R. rosea) is one of the most beneficial medicinal plants and it is studied as an adaptogen. This study aims to evaluate the neuroprotective activity of compounds extracted from the root of R. rosea against methylglyoxal (MG)-induced apoptosis in neuro-2A (N2A) cells. The root of R. rosea was extracted with ethanol and partitioned with water, ethyl acetate, and n-butanol fractions to evaluate acetylcholinesterase (AChE) inhibitory activity and neuroprotective activity. The ethyl acetate fraction exhibited the highest values of AChE inhibitory activity (49.2% ± 3%) and cell viability (50.7% ± 4.8%) for neuroprotection. The structure identification of the most potential fraction (ethyl acetate fraction) revealed 15 compounds, consisting of three tannins, five flavonoids, and seven phenolics by infrared spectroscopy, nuclear magnetic resonance, and mass spectroscopy. All compounds were evaluated for their neuroprotective activity. Salidroside had the most potential neuroprotective activity. Gallic acid and methyl gallate had potential cytotoxicity in N2A cells. This study showed that R. rosea might have potential neuroprotective activities.

Highlights

  • Alzheimer’s disease (AD) is the most common cause of dementia among older adults

  • Our research focused on activity-tracking strategies to analyze different parts of R. rosea

  • At 500 μg/mL, the ethyl acetate fraction of

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Summary

Introduction

Alzheimer’s disease (AD) is the most common cause of dementia among older adults. AD is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills. All drug developments for AD have failed; developing effective drugs is urgent. Methylglyoxal (MG) is a reactive dicarbonyl intermediate and the most potent precursor for the formation of advanced glycation end-products (AGEs) [1]. AGEs are stable end-products formed in cells, and the accumulation of AGEs in the brain might contribute to neuronal inflammation [2]. MG is an important factor in oxidative stress and neurodegeneration [3]. The brain has very high energy requirements and high glucose demand in order to maintain neural cell function

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