Title

 

Authors

F. Morroni, A. Tarozzi, C. Bolondi, J.M. Zolezzi Moraga, G. Cantelli Forti and P. Hrelia.
             
Dept. of Pharmacology, Alma Mater Studiorum - University of Bologna, Italy. 
 

 

Abstract

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra and subsequent loss of dopaminergic input into the striatum. Breakdown of dopaminergic signalling within the nigrostriatal pathway is believed to underlie many of the motor symptoms associated with PD, such as bradykinesia, muscular rigidity, postural instability, and tremor. Current therapies for motor symptoms of PD are based on dopamine replacement. However, these therapies do not affect disease progression and the issue of dopaminergic neuron loss is still unsolved. Here, we describe the effect of sulforaphane (SFN), a naturally occurring compound present in high levels in cruciferous vegetables, on brain protection against the parkinsonian toxin 6-hydroxydopamine (6-OHDA). In our study, we employed a pharmacological mouse model of PD, in which we unilaterally injected 6-OHDA in the striatum. After brain lesion, one month of intraperitoneal administration of SFN (5 mg/kg) rescued motor impairments, as shown by rotarod performance and rotational behavior. Moreover, SFN provided protection against 6-OHDA-induced death of dopaminergic neurons. SFN neuroprotection was observed to be mediated by the ability of SFN to modulate the extracellular signal regulated kinase 1 and 2, known as kinases involved in pro-survival neuronal pathways. Our findings on the behavioral and pathophysiological improvements offered by post-injury SF administration suggest that this compound is a promising therapeutic option for the treatment ofPD either alone or, it should be reasonable, as neuroprotective strategy together with dopamine replacement therapy.