Recent Updates in Redox Regulation and Free Radical Scavenging Effects by Herbal Products in Experimental Models of Parkinson’s Disease

Abstract

Parkinson’s disease (PD) is a complex multifactorial disease marked by extensive neuropathology in the brain with selective yet prominent and progressive loss of mid-brain dopaminergic neurons. The etiological factors involved in the development of PD are still elusive, but oxidative stress arising when reactive oxygen species (ROS) exceed amounts required for normal redox signaling is considered one of the major factors. ROS cause oxidative damage to proteins, lipids, and DNA and are one of the most prominent factors related to neurodegeneration. Pre-clinical and clinical studies clearly demonstrate the effectiveness of oxidative stress in the pathogenesis of PD. Therefore, regulation of redox signaling and inhibiting excess ROS would contribute greatly not only to extend longevity but also to ameliorate the progression of dopaminergic cell death seen in patients with PD. Several herbal products are beneficial for maintaining nerve cell function and for treating various neurodegenerative disorders by reducing oxidative stress. Here, we summarize the recent knowledge concerning promising herbs that have shown significant beneficial effects based on regulation of redox status and ROS inhibition in toxin-induced PD models.

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

“…for midbrain dopaminergic neurons and other neuronal and nonneuronal cell populations (Dumont and Beal, 2011;Ebadi et al, 1996;Fariss and Zhang, 2003;Koppula et al, 2012aKoppula et al, , 2012bMayo et al, 2005;Sharma and Nehru, 2013). However, the results of human clinical trials are inconsistent in slowing down disease progression, but there is still hope that improved antioxidant mimetics that better target ROS production pathways might prove beneficial.…”

Oleuropein Prevents Neuronal Death, Mitigates Mitochondrial Superoxide Production and Modulates Autophagy in a Dopaminergic Cellular Model

“…Although current pharmacological treatments aim to appease symptoms and to slow disease progression, tremendous efforts are presently deployed to formulate strategies that address neuronal death, either by preventing it (neuroprotection) or stopping it (neurorescue) [21,23,24,25,26]. Following this line of evidence, several natural phenolic compounds have already demonstrated their neuroprotective properties in the context of neurodegeneration.…”

Protective effect of green tea against neuro-functional alterations in rats treated with MnO2nanoparticles

“…These act, on the one hand, as radical scavengers, and on the other as metal chelators . This way, they can counteract several nervous system damaging effects of Mn, both related (mitochondrial damage) and unrelated (interference with glutamate turnover) to oxidative stress.…”

“…The neuroprotective effect of catechins and other tea flavonoids is based on antioxidant and metal chelating activity; but beyond acting directly as radical scavengers, they also activate transcription factors and antioxidant enzymes . Regarding the prevalence of chronic degenerative central nervous system (CNS) diseases and the popularity of tea, this protective effect has been extensively studied, and the possible beneficial effect of phytochemicals in neuroprotection has been mentioned repeatedly …”

“…3 Regarding the prevalence of chronic degenerative central nervous system (CNS) diseases and the popularity of tea, this protective effect has been extensively studied, and the possible beneficial effect of phytochemicals in neuroprotection has been mentioned repeatedly. 4,5 One of the toxic heavy metals often encountered in industrial settings is manganese (Mn). Significant exposure and health damage have been described first of all in the metal industry, most frequently in welding jobs, but also in the manufacture of zinc-carbon and alkaline dry cells.…”