Neuroprotective effects of catechin and quercetin in experimental Parkinsonism through modulation of dopamine metabolism and expression of IL-1β, TNF-α, NF-κB, IκKB, and p53 genes in male Wistar rats.

The neurobehavioral, brain redox-stabilizing and neurochemical modulatory properties of catechin and quercetin in rotenone-induced Parkinsonism, and the involvement of NF-κB-mediated inflammation, were investigated. Male Wistar rats subcutaneously administered with multiple doses of 1.5 mg/kg rotenone were post-treated with 5-20 mg/kg catechin or quercetin. This was followed by neurobehavioral evaluation, biochemical estimations, and assessment of neurotransmitter metabolism in the striatum. Expression of genes involved in the canonical pathway for the activation of NF-κB mediated inflammation (IL-1β, TNF-α, NF-κB, and IκKB) and the pro-apoptotic gene, p53, in the striatum was determined by RT-qPCR. Catechin and quercetin mitigated neurobehavioral deficits caused by rotenone. Both flavonoids attenuated striatal redox stress and neurochemical dysfunction, optimized disturbed dopamine metabolism, and improved depletion of neuron density caused by rotenone toxicity. While administration of catechin produced a more pronounced attenuating effect on IL-1β, TNF-α, and p53 genes, the attenuating effect of quercetin (20 mg/kg) was more pronounced on NF-κB and IκKB gene expressions when compared to the group administered with rotenone only. Comparatively, quercetin demonstrated superior protection against rotenone neurotoxicity. It is concluded that catechin and quercetin have potential relevance in Parkinson's disease therapy through amelioration of redox stress, optimization of dopamine metabolism, and modulation of anti-inflammatory and anti-apoptotic pathways.