Planta Med 2008; 74 - PA210
DOI: 10.1055/s-0028-1084208

Syringin from Fraxinus rhynchophylla Hance inhibit the apoptotic neuronal cell death induced by Aβ25–35

EJ Yang 1, HJ Kim 1, HJ Park 1, HY Ku 1, DG Lee 1, YH Seong 2, KS Song 1
  • 1Division of Applied Biology & Chemistry, College of Agriculture and Life Sciences, Kyungpook National University, 1370, Sankyuk-Dong, Daegu 702–701, Korea
  • 2College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 361–763, Korea

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive degeneration and loss of neuronal cells in the brain. β-Amyloid peptide (Aβ) is produced by proteolysis of amyloid precursor protein (APP), and its accumulation in the senile plaque is the major hallmark of AD pathogenesis [1, 2, 3]. Various experimental evidence support that Aβ plaque can induce neurotoxic effect on neuronal cells [4].

In the course of screening of anti-dementia agents from medicinal plants, the ethanolic extract of Fraxinus rhynchophylla Hance showed neuroprotective effect against Aβ25–35-induced cytotoxicity in cultured B103 cells. The extract was partitioned with dichloromethane (CH2Cl2), n-butanol (n-BuOH), and water, successively. The repeated chromatographic separation afforded an active compound, and its chemical structure was elucidated as syringin by 1H- and 13C-NMR and LC-MS. Its effects on apoptotic cell death were determined by MTT, H2DCF-DA and caspase-3 activity assay. As results, syringin significantly increased B103 cell viability up to 79.16% at 20µM in the presence of 12.5µM of Aβ25–35, and it remarkably decreased Aβ25–35-induced reactive oxygen species (ROS) generation up to 92.87% at the same concentration. In addition, the activity of caspase-3, an enzymatic major marker of apoptosis, was decreased up to 39.75% at 25µM.

These results indicate that syringin and ethanolic extracts from Fraxinus rhynchophylla Hance could be a promising agent for anti-dementia.

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