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Review
. 2015:2015:314560.
doi: 10.1155/2015/314560. Epub 2015 Oct 20.

Protective Mechanisms of Flavonoids in Parkinson's Disease

Kasthuri Bai Magalingam  1 , Ammu Kutty Radhakrishnan  1 , Nagaraja Haleagrahara  2
Affiliations
Review

Protective Mechanisms of Flavonoids in Parkinson's Disease

Kasthuri Bai Magalingam et al. Oxid Med Cell Longev. 2015.

Abstract

Parkinson's disease is a chronic, debilitating neurodegenerative movement disorder characterized by progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta region in human midbrain. To date, oxidative stress is the well accepted concept in the etiology and progression of Parkinson's disease. Hence, the therapeutic agent is targeted against suppressing and alleviating the oxidative stress-induced cellular damage. Within the past decades, an explosion of research discoveries has reported on the protective mechanisms of flavonoids, which are plant-based polyphenols, in the treatment of neurodegenerative disease using both in vitro and in vivo models. In this paper, we have reviewed the literature on the neuroprotective mechanisms of flavonoids in protecting the dopaminergic neurons hence reducing the symptoms of this movement disorder. The mechanism reviewed includes effect of flavonoids in activation of endogenous antioxidant enzymes, suppressing the lipid peroxidation, inhibition of inflammatory mediators, flavonoids as a mitochondrial target therapy, and modulation of gene expression in neuronal cells.

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Figures

Figure 1
Figure 1
Simplified depiction of ROS and MAPK-induced cytotoxicity. External stimuli including neurotoxin or lipopolysaccharide could generate ROS that is able to suppress the endogenous antioxidant enzymes particularly superoxide dismutase, glutathione peroxidase, and catalase and leads to increase in lipid peroxidation and cell death. The ROS has the ability to directly cause lipid peroxidation and cellular damage as well affecting the mitochondria metabolism, which suppresses the Bcl-Bax ratio and result in leakage of cytochrome-c from mitochondria and eventually cell death. The presence of external stimuli activates MAPK-induced inflammatory mediators including JNK and c-JUN that cause activation of proapoptotic caspases, namely, Caspase 3 and Caspase 9; and the effect is cellular apoptosis. The MAPK family is also responsible in initiating the NF-κB induced expression of proinflammatory cytokine genes (iNOS, TNF-α, and ILIβ). The symptoms of Parkinson's disease occur as a result of neurodegeneration of dopamine producing neurons.
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