agathisflavone and Parkinson-Disease

Flavonoids have been suggested to protect dopaminergic neurons in Parkinson's disease based on studies that used exogenous neurotoxins. In this study, we tested the protective ability of agathisflavone in SH-SY5Y cells exposed to the endogenous neurotoxin aminochrome. The ability of aminochrome to induce loss of lysosome acidity is an important mechanism of its neurotoxicity. We demonstrated that the flavonoid inhibited cellular death and lysosomal dysfunction induced by aminochrome. In addition, we demonstrated that the protective effect of agathisflavone was suppressed by antagonists of estrogen receptors (ERα and ERβ). These results suggest lysosomal protection and estrogen signaling as mechanisms involved in agathisflavone neuroprotection in a Parkinson's disease study model.

Topics: Biflavonoids; Cell Death; Dopaminergic Neurons; Humans; Neuroprotection; Neurotoxicity Syndromes; Neurotoxins; Parkinson Disease