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 Petasites japonicus (Siebold & Zucc.) Maxim. (PL), called butterbur and traditionally used in folk medicine, show neuroprotective action against Aβ25⁻35 plaque neurotoxicity in vitro and in vivo. We found that PL protected Aβ25⁻35 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 Aβ25⁻35 plaque-injected AD mouse models. Moreover, administration of PL diminished Aβ25⁻35 plaque-induced synaptic dysfunction and memory impairment in mice. These findings lead us to suggest that PL can protect neurons against Aβ25⁻35 plaque-induced neurotoxicity and thus may be a potential candidate to regulate the progression of AD.
Keywords: Alzheimer’s disease; Petasites japonicus; amyloid beta; butterbur; memory.