Ligularia fischeri Extract Protects Against Oxidative-Stress-Induced Neurotoxicity in Mice and PC12 Cells
Authors:
- 1 November 2014
- journal article
- Published by SAGE Publications in Journal of Medicinal Food
- Vol. 17 (11) , 1222-1231
Abstract
Alzheimer's disease (AD) is pathologically characterized by the presence of amyloid plaques in brain and the overproduction of amyloid beta (A β ), leading to learning and memory impairment and intense oxidative stress. In this study, the protective effect of Ligularia fischeri extract was investigated using PC12 cells. L. fischeri extract attenuated hydrogen-peroxide-induced DNA fragmentation in cells. In vivo behavioral tests were performed to examine the effects of the extract on amyloid- β peptide 1-42 -induced impairment of learning and memory in mice. A diet containing the extract increased alternation behaviors in the Y-maze test and step-through latency of passive avoidance task. Moreover, we found that consumption of the extract decreased lipid peroxidation in a biochemical study of brain tissue in mice. High-performance liquid chromatography was used to identify the active compounds in the extract. These results suggest that L. fischeri extract could be protective against A β -induced neurotoxicity, possibly due to the antioxidative capacity of its constituent, 3- O -caffeoylquinic acid.Keywords
This publication has 40 references indexed in Scilit:
- Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's diseaseTrends in Molecular Medicine, 2008
- Mechanisms of Aβ mediated neurodegeneration in Alzheimer's diseaseThe International Journal of Biochemistry & Cell Biology, 2008
- Roles of amyloid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairmentFree Radical Biology and Medicine, 2007
- Alzheimer’s amyloid β-peptide (1–42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptideNeurobiology of Aging, 2004
- Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer’s disease brain contribute to neuronal death1Neurobiology of Aging, 2002
- β-Amyloid Fragment 25–35 Causes Mitochondrial Dysfunction in Primary Cortical NeuronsNeurobiology of Disease, 2002
- Free radical-induced damage to DNA: mechanisms and measurement 1,2 1This article is part of a series of reviews on “Oxidative DNA Damage and Repair.” The full list of papers may be found on the homepage of the journal. 2Guest Editor: Miral DizdarogluFree Radical Biology and Medicine, 2002
- Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptideTrends in Molecular Medicine, 2001
- Reactive oxygen species in Alzheimer's diseaseEuropean Neuropsychopharmacology, 1999
- Amyloid β-protein toxicity and oxidative stress in Alzheimer's diseaseCell and tissue research, 1997