期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 22, 期 1, 页码 151-159出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2014.06.018
关键词
Amyloid-beta; Alzheimer's disease; PC12; Apoptosis; MAPK; Notoginsenoside R1
资金
- China Postdoctoral Science Foundation [2012M510360]
- Major Scientific and Technological Special Project for 'Significant New Drugs Formulation' [2012ZX09501001, 20122X09301002-001]
Progressive accumulation of amyloid-beta (A beta) is a pathological hallmark of Alzheimer's disease (AD). A beta increases free radical production in neuronal cells, leading to oxidative stress and cell death. An intervention that would reduce A beta-related neurotoxicity through free radical reduction could advance the treatment of AD. Notoginsenoside R1 (NR1), the major and most active ingredient in the herb Panax notoginseng, can reduce reactive oxygen species and confer some neuroprotective effects. Here, NR1 was applied in a cell-based model of Alzheimer's disease. Cell viability, cell death, reactive oxygen species generation, and mitochondrial membrane potential were assessed in cultured PC12 neuronal cells incubated with A beta(25-35). In this model, A beta was neurotoxic and induced necrosis and apoptosis; however, NR1 significantly counteracted the effects of A beta by increasing cell viability, reducing oxidative damage (including apoptosis), restoring mitochondrial membrane potential, and suppressing stress-activated MAPK signaling pathways. These results promise a great potential agent for Alzheimer's disease and other A beta pathology-related neuronal degenerative disease. (C) 2014 Elsevier B.V. All rights reserved.
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