Neuroprotective Effects of Polyphenol-Rich Corinthian Currant Against a Rotenone Parkinson’s Disease Model: Mitigation of MAO-B and Pro-Inflammatory Cytokines Upregulation in Motor and Limbic Brain Regions

Parkinson’s disease (PD) is a progressive neurodegenerative disorder of motor function, while at advanced stages it includes memory deficits and neuropsychiatric conditions. It is characterized primarily by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and reduced dopamine levels in the striatum. Accumulating evidence highlights the role of polyphenols against oxidative stress and neuroinflammatory processes, underlying key factors of PD pathogenesis. The present study used a rotenone rat model to determine the involvement of inflammatory cytokines in the basal ganglia, hippocampus, basolateral amygdala, and prefrontal cortex and to evaluate the potential of black Corinthian currant, a fruit abundant in antioxidant polyphenols, to attenuate brain inflammatory responses. Rotenone is known to trigger oxidative stress by inhibiting mitochondrial complex I and thus induce dopaminergic neurodegeneration, further amplified by inflammation. Our findings clearly demonstrated that rotenone treatment resulted in significant increases in pro-inflammatory cytokines as well as MAO-B expression within the rat brain motor and limbic regions. Importantly, dietary supplementation with black Corinthian currant mitigated rotenone-induced overexpression of IL-1β, TNFα, and MAO-B. Moreover, double immunofluorescence suggested the microglial localization of these inflammatory markers in SNpc. Overall, our data highlight the neuroprotective potential of dietary Corinthian currant polyphenols, modulating glial-mediated neuroinflammation in a rotenone PD model.