Theaflavin ameliorates behavioral deficits, biochemical indices and monoamine transporters expression against subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of Parkinson's disease.

Evidence from clinical and experimental studies indicates that degeneration of nigrostriatal dopaminergic neurons is a pathological hallmark of Parkinson's disease (PD). The present study was designed to investigate the neuroprotective potential of theaflavin (TF) on oxidative stress, monoamine transporters and behavioral abnormalities in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurodegeneration. TF, a black tea polyphenol, has been known to possess neuroprotective effects against ischemia, Alzheimer's disease and other neurodegenerative disorders, but the mechanisms underlying its beneficial effects on MPTP-induced dopaminergic neurodegeneration are poorly defined. Administration of MPTP (30 mg/kg bw for four consecutive days) led to increased oxidative stress and reduced behavior patterns (open field, rotarod and hang test), nigrostriatal dopamine transporter (DAT) (immunohistochemistry and Western blot) and vesicular monoamine transporter 2 (VMAT2) (Western blot) expressions. Pre-treatment with TF reduces oxidative stress, improves motor behavior and expression of DAT and VMAT2 in striatum and substantia nigra. These results indicate that TF might be beneficial in mitigating MPTP-induced damage of dopaminergic neurons, possibly via its neuroprotective and its antioxidant potential.