Neuroprotective effect of α-mangostin in MPTP-induced parkinson's disease in mice: mitochondrial enzymes analysis

Parkinson's disease (PD) is one of the common neurodegenerative disease and is considered to be the second most prevalence disease after Alzheimer's disease. PD is characterized with loss of dopaminergic neurons in brain that causes effect to motor symptoms and also non-motor symptoms. Pathogenesis of PD cannot be described clearly. However, PD can be divided to idiopathic and sporadic based on the factors. There is no cure for PD. Emergence of modem drugs are progressively increasing in treating the symptoms of PD. Side effects due to consumption of the modem drugs outweigh their benefits in treating the symptoms. Hence, our study aims to explore a potential compound derived from natural source (α-mangostin) that can prevent and protect progressive event of the symptoms. In our study, a PD mouse model {MPTP­ induced neurotoxicity) was treated with a compound found from the pericarp of mangosteen, o-mangostin. MPTP metabolite, MPP+ that causes apoptotic cell death and inhibits the membrane-bound complexes ( complex I, II, III and IV) in the mitochondria and thus inhibit the electron transfer of electron transport chain, followed by ATP depletion. High dose of α-mangostin (6 mg/kg, p.o.) showed probable effect due to its ability in increasing activities of all of the mitochondrial complexes. In addition, L-NAME, inhibitor of nitric oxide synthase, was used to modulate level of nitric oxide. Decreased level of NO was found to inhibit oxidative stress and strengthen the effect produced by n-mangostin. Administration of L­-NAME (5 mg/kg, i.p.) with α-rnangostin (3 mg/kg, p.o.) showed increase of complexes activities. In conclusion, α-mangostin is a potential compound to prevent progression of PD.