The investigation of the effect of cortexin on learning and behavior via HMGB1 in rats with Parkinson's model

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by neuroinflammation, oxidative stress, and dopaminergic neuronal loss. In recent years, the high mobility group box-1 (HMGB1) protein has been shown to play a critical role in PD pathogenesis by enhancing neuroinflammatory responses through Toll-like receptor 4 (TLR4) and the receptor for advanced glycation end products (RAGE). This thesis aimed to investigate the effects of cortexin, a peptide complex reported to exhibit neuroprotective and anti-inflammatory properties, on HMGB1-mediated neuroprotection in a rotenone-induced PD animal model. In this experimental study conducted on male Wistar albino rats, a PD model was established through systemic rotenone administration, followed by cortexin treatment. The effects of cortexin on behavioral performance, cortical neuronal integrity, oxidative stress levels, and HMGB1 signaling pathways were evaluated. Significant improvements in motor behavioral tests were observed in the cortexin-treated group, and histological analyses confirmed reduced neuronal loss in the cortex. Additionally, cortexin administration resulted in increased HMGB1 levels. These findings suggest that cortexin may exert neuroprotective effects in PD through mechanisms involving HMGB1. Overall, the study indicates that cortexin may be a potential therapeutic candidate for PD and highlights the importance of HMGB1 signaling as a promising pharmacological target.