Irisflorentin improves α-synuclein accumulation and attenuates 6-OHDA-induced dopaminergic neuron degeneration, implication for Parkinson's disease therapy
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Abstract
[[abstract]]Parkinson’s disease (PD) is a degenerative disorder of the central nervous system that is characterized by
progressive loss of dopaminergic neurons in the substantia nigra pars compacta as well as motor impairment.
Aggregation of α-synuclein in neuronal cells plays a key role in this disease. At present, therapeutics for PD
provides moderate symptomatic benefits, but it is not able to delay the development of the disease. Current
efforts toward the treatment of PD are to identify new drugs that slow or arrest the progressive course of PD
by interfering with a disease-specific pathogenetic process in PD patients. Irisflorentin derived from the
roots of Belamcanda chinensis (L.) DC. is an herb which has been used for the treatment of inflammatory
disorders in traditional Chinese medicine. The purpose of the present study was to assess the potential for
irisflorentin to ameliorate PD in Caenorhabditis elegans models. Our data reveal that irisflorentin prevents
α-synuclein accumulation in the transgenic Caenorhabditis elegans model and also improves dopaminergic
neuron degeneration, food-sensing behavior, and life-span in a 6-hydroxydopamine-induced Caenorhabditis
elegans model, thus indicating its potential as a anti-parkinsonian drug candidate. Irisflorentin may exert
its effects by promoting rpn-3 expression to enhance the activity of proteasomes and down-regulating egl-1
expression to block apoptosis pathways. These findings encourage further investigation on irisflorentin as a
possible potent agent for PD treatment