Cilostazol Mediated Nurr1 and Autophagy Enhancement: Neuroprotective Activity in Rat Rotenone PD Model

In conclusion, cilostazol could be a promising candidate for PD treatment through modulating Nurr1 expression, as well as SIRT-1/autophagy, and GSK-3β/apoptosis cross-regulation.Graphical AbstractIn the rat rotenone model of Parkinson ’s disease (PD), Nurr1 expression was downregulated, GSK-3β was activated, and autophagic flux was inhibited. Those deleterious effects were associated with deteriorated motor functions, striatal TH content, enhanced inflammatory state, and apoptotic cascade. Cilostazol, a phosphodiesterase-3 inh ibitor, exerted a potential protective effect against PD through Nurr1 enhancement, GSK-3β/apoptosis modulation, and SIRT-1/autophagy enhancement. Nurr1 nuclear receptor related 1, TH tyrosine hydroxylase, NF-κB nuclear factor κB, TNFα tumor necrosis factor alpha, ILs interleukins, GSK-3β glyco gen synthase kinase 3 beta, SIRT-1 sirtuin 1.
Source: Molecular Neurobiology - Category: Neurology Source Type: research