Butterbur Leaves Attenuate Memory Impairment and Neuronal Cell Damage in Amyloid Beta-Induced Alzheimer's Disease Models

• Published in: International journal of molecular sciences Vol. 19; no. 6; p. 1644
• Main Authors: Kim, Namkwon, Choi, Jin Gyu, Park, Sangsu, Lee, Jong Kil, Oh, Myung Sook
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.06.2018; MDPI
• Subjects: Alzheimer Disease - complications; Alzheimer's disease; amyloid beta; Amyloid beta-Peptides; Animal models; Animals; Apoptosis; butterbur; Cell death; Cells, Cultured; Cyclic AMP; Cyclic AMP response element-binding protein; Degeneration; Disease Models, Animal; Heme; Heme oxygenase (decyclizing); Impairment; Leaves; Male; Memory; Memory Disorders - drug therapy; Memory Disorders - etiology; Memory Disorders - prevention & control; Mice; Neurodegeneration; Neurons - drug effects; Neurons - metabolism; Neurons - pathology; Neuroprotection; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neurotoxicity; Oxidative Stress; Oxygenase; Peptide Fragments; Petasites - chemistry; Petasites japonicus; Plant Extracts - pharmacology; Plant Extracts - therapeutic use; Plant Leaves - chemistry; Plaque, Amyloid; Proteins; Quinine; butterbur; memory; Alzheimer’s disease; amyloid beta; Petasites japonicus
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms19061644

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease, and is characterized by the accumulation of amyloid beta (Aβ) as a pathological hallmark. Aβ plays a central role in neuronal degeneration and synaptic dysfunction through the generation of excessive oxidative stress. In the present study, we explored whether leaves of (Siebold & Zucc.) Maxim. (PL), called butterbur and traditionally used in folk medicine, show neuroprotective action against Aβ plaque neurotoxicity in vitro and in vivo. We found that PL protected Aβ plaque-induced neuronal cell death and intracellular reactive oxygen species generation in HT22 cells by elevating expression levels of phosphorylated cyclic AMP response element-binding protein, heme oxygenase-1, and NAD(P)H quinine dehydrogenase 1. These neuroprotective effects of PL were also observed in Aβ plaque-injected AD mouse models. Moreover, administration of PL diminished Aβ plaque-induced synaptic dysfunction and memory impairment in mice. These findings lead us to suggest that PL can protect neurons against Aβ plaque-induced neurotoxicity and thus may be a potential candidate to regulate the progression of AD.