Abstract
Parkinson’s disease (PD) is one of the most prevalent and debilitating neurodegenerative conditions, and is currently on the rise. Several dysregulated pathways are behind the pathogenesis of PD; however, the critical targets remain unclear. Accordingly, there is an urgent need to reveal the key dysregulated pathways in PD. Prevailing reports have highlighted the importance of mitochondrial and cross-talked mediators in neurological disorders, genetic changes, and related complications of PD. Multiple pathophysiological mechanisms of PD, as well as the low efficacy and side effects of conventional neuroprotective therapies, drive the need for finding novel alternative agents. Recently, much attention has been paid to using plant secondary metabolites (e.g., flavonoids/phenolic compounds, alkaloids, and terpenoids) in the modulation of PD-associated manifestations by targeting mitochondria. In this line, plant secondary metabolites have shown promising potential for the simultaneous modulation of mitochondrial apoptosis and reactive oxygen species. This review aimed to address mitochondria and multiple dysregulated pathways in PD by plant-derived secondary metabolites.
Highlights
Humans have always been affected by various neurological complications [1,2]
The findings suggest that silibinin has such benefits in MPTP-induced models of Parkinson’s disease (PD) achieved through increasing the stability of mitochondrial membrane potential [49]
A subset of phenols, including ellagic acid and ferulic acid, affected mitochondria and thereby protected them from reactive oxygen species (ROS)-related pathways [32]. Protocatechuic aldehyde is another phenolic acid gained from the root of Salvia miltiorrhiza, which has a protective effect on mitochondria by blocking ROS production and keeping the activity of complex I in MPP+ -incubated SH-SY5Y cells evaluated in an in vitro experiment [15]
Summary
Sajad Fakhri 1,† , Sadaf Abdian 2,† , Seyede Nazanin Zarneshan 2 , Esra Küpeli Akkol 3 , Mohammad Hosein Farzaei 1, * and Eduardo Sobarzo-Sánchez 4,5, *.
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