Effects of Brain Factor‑7® against motor deficit and oxidative stress in a mouse model of MPTP‑induced Parkinson's disease

Oxidative stress is strongly implicated in the pathogenesis of Parkinson's disease (PD) through degeneration of dopaminergic neurons. The present study was designed to investigate the underlying mechanisms and therapeutic potential of Brain Factor‑7^® (BF‑7^®), a natural compound in silkworm, in a mouse model of PD induced by 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP). MPTP (20 mg/kg) was intraperitoneally injected into mice to cause symptoms of PD. Mice were orally administered BF‑7^® (a mixture of silk peptides) before and after MPTP treatment. Rotarod performance test was used to assess motor performance. Fluoro‑Jade B staining for neurons undergoing degeneration and immunohistochemistry of tyrosine hydroxylase for dopaminergic neurons, 4‑hydroxy‑2‑nonenal (4HNE) for lipid peroxidation, 8‑hydroxy‑2'‑deoxyguanosine (8OHdG) for DNA damage and superoxide dismutase (SOD) 1 and SOD2 for antioxidative enzymes in the pars compacta of the substantia nigra were performed. Results showed that BF‑7^® treatment significantly improved MPTP‑induced motor deficit and protected MPTP‑induced dopaminergic neurodegeneration. Furthermore, BF‑7^® treatment significantly ameliorated MPTP‑induced oxidative stress. Increased 4HNE and 8OHdG immunoreactivities induced by MPTP were significantly reduced by BF‑7^®, whereas SOD1 and SOD2 immunoreactivities decreased by MPTP were significantly enhanced by BF‑7^®. In conclusion, BF‑7^® exerted protective and/or therapeutic effects in a mouse model of PD by decreasing effects of oxidative stress on dopaminergic neurons in the substantia nigra pars compacta.