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Abstract Title:

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

Abstract Source:

Int Immunopharmacol. 2014 Sep ;22(1):151-9. Epub 2014 Jun 24. PMID: 24975829

Abstract Author(s):

Bo Ma, Xiangbao Meng, Jing Wang, Jing Sun, Xiaoyu Ren, Meng Qin, Jie Sun, Guibo Sun, Xiaobo Sun

Article Affiliation:

Bo Ma

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 (includingapoptosis), 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.

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Sayer Ji
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