EGCG Mediates Neuroprotection in a Parkinson’s Disease Model via a Caspase-3-Independent Pathway

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss in the substantia nigra, mainly due to apoptosis triggered by reactive oxygen species (ROS) and α-synuclein aggregation. Investigating natural compounds with anti-apoptotic potential is essential for developing neuroprotective strategies. This study aimed to evaluate the effect of epigallocatechin gallate (EGCG) from Camellia sinensis on neuronal apoptosis markers, caspase-3 and Bcl-2, in a rat model of Parkinson’s disease. Thirty male Wistar rats were divided into five groups, including normal and PD models induced by intraperitoneal 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP). EGCG was administered to the treatment groups, while control groups received placebo. On the seventh day, rats were sacrificed and substantia nigra samples were examined immunohistochemically for caspase-3 and Bcl-2 expression. EGCG administration did not significantly alter caspase-3 or Bcl-2 expression (p?> 0.05) compared to placebo; however, neuronal degeneration was significantly reduced in EGCG-treated normal rats (F = 4.491, p < 0.05). EGCG exhibits neuroprotective effects independent of caspase-3 and Bcl-2 modulation, suggesting a potential caspase-3-independent pathway in neuroprotection.