Protective Mechanisms of Flavonoids in Parkinson’s Disease

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-B induced expression of proinflammatory cytokine genes (iNOS, TNF-, and ILI). The symptoms of Parkinson’s disease occur as a result of neurodegeneration of dopamine producing neurons.