Neuroprotective effect of epigallocatechin gallate extract of Camellia sinensis on α-Synuclein, PKCδ, and neuronal degeneration in an MPTP-induced rat model of Parkinson’s disease

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Parkinson’s disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuronal loss, primarily due to α-synuclein accumulation and apoptosis-related signaling. Epigallocatechin gallate (EGCG), a potent polyphenol in Camellia sinensis, shows neuroprotective properties, but its mechanisms in PD remain incompletely understood. This study aimed to evaluate the neuroprotective effect of epigallocatechin gallate (EGCG) extract of Camellia sinensis on serum α-synuclein concentration, serum PKCδ concentration, and neuronal degeneration in an MPTP-induced rat model of Parkinson’s disease, and to examine whether the observed protection may be associated with modulation of apoptosis-related signaling. Forty male Wistar rats were randomly allocated into five groups: normal control (K0), normal placebo (K1), PD placebo (K2), normal + EGCG (K3), and PD + EGCG (K4). Parkinsonism was induced in K2 and K4 using MPTP (16 mg/kg BW). EGCG (30 mg/kg BW/day) was administered orally for 7 days. Serum α-synuclein and serum PKCδ concentrations were measured by ELISA, and neuronal degeneration in the substantia nigra was assessed histologically. Serum α-synuclein concentration differed significantly among the groups and was highest in the PD placebo group, whereas the PD + EGCG group showed one of the lowest values. Serum PKCδ concentration also differed significantly among groups; however, the reduction in the PD + EGCG group was not significantly different from that in the PD placebo group. Neuronal degeneration tended to be lower in the PD + EGCG group than in the PD placebo group, but the difference was not statistically significant. EGCG showed neuroprotective potential in MPTP-induced rats, as reflected by reduced α-synuclein concentration and a tendency toward lower PKCδ concentration and neuronal degeneration. However, because PKCδ and histopathological improvement were not significantly different between the PD placebo and PD + EGCG groups, additional mechanisms beyond PKCδ-related apoptosis are likely to contribute to the observed neuroprotective effect. This study supports Sustainable Development Goal 3 (Good Health and Well-being) by contributing to research on neurodegenerative disease prevention and management.