2. Academic Validation
  3. Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation

Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation

  • Int Immunopharmacol. 2014 Sep;22(1):151-9. doi: 10.1016/j.intimp.2014.06.018.
Bo Ma 1,  Xiangbao Meng 1,  Jing Wang 1,  Jing Sun 1,  Xiaoyu Ren 2,  Meng Qin 1,  Jie Sun 1,  Guibo Sun 3,  Xiaobo Sun 4
Affiliations

Affiliations

  • 1 Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, 151, Malianwa North Road, Haidian District, Beijing 100193, PR China.
  • 2 Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, 151, Malianwa North Road, Haidian District, Beijing 100193, PR China; Eastern Liaoning University, No. 325 Wenhua Street, Yuanbao District, Dandong Liaoning 118003, PR China.
  • 3 Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, 151, Malianwa North Road, Haidian District, Beijing 100193, PR China. Electronic address: guibo_sun610@126.com.
  • 4 Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, 151, Malianwa North Road, Haidian District, Beijing 100193, PR China. Electronic address: xiaobo_sun610@126.com.
PMID: 24975829 DOI: 10.1016/j.intimp.2014.06.018
Abstract

Progressive accumulation of Amyloid-β (Aβ) is a pathological hallmark of Alzheimer's disease (AD). Aβ increases free radical production in neuronal cells, leading to oxidative stress and cell death. An intervention that would reduce Aβ-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 Aβ(25-35). In this model, Aβ was neurotoxic and induced necrosis and apoptosis; however, NR1 significantly counteracted the effects of Aβ 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 Aβ pathology-related neuronal degenerative disease.

Keywords

Alzheimer's disease; Amyloid-β; Apoptosis; MAPK; Notoginsenoside R1; PC12.

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