Bacopa monnieri Phytochemicals Mediated Synthesis of Platinum Nanoparticles and Its Neurorescue Effect on 1-Methyl 4-Phenyl 1,2,3,6 Tetrahydropyridine-Induced Experimental Parkinsonism in Zebrafish
Current discovery demonstrates the rapid formation of platinum nanoparticles using leaf extract of a neurobeneficial plant, Bacopa monnieri (BmE). The nanoparticles (BmE-PtNPs) were stabilized and then coated with varied phytochemicals present within the leaf extract. These nanoparticles demonstrated the same activity of Complex I, as that of oxidizing NADH to NAD+ using a spectrophotometric method. This suggests that BmE-PtNPs are a potential medicinal substance for oxidative stress mediated disease with suppressed mitochondrial complex I, namely, Parkinson's disease (PD). Hence, the neuroprotective potentials of the phytochemical coated nanoparticle were explored in 1-methyl 4-phenyl 1,2,3,6 tetrahydropyridine- (MPTP-)induced experimental Parkinsonism in zebrafish model. BmE-PtNPs pretreatment significantly reversed toxic effects of MPTP by increasing the levels of dopamine, its metabolites, GSH and activities of GPx, catalase, SOD and complex I, and reducing levels of MDA along with enhanced locomotor activity. Taken together, these findings suggest that BmE-PtNPs have protective effect in MPTP-induced neurotoxicity in this model of Parkinson's disease via their dual functions as mitochondrial complex I and antioxidant activity. 1. Introduction Parkinson’s disease (PD) is a neurodegenerative disease of dopamine (DA) neurons in substantia nigra characterized predominantly by resting tremors, bradykinesia, muscular rigidity, and postural instability, along with several nonmotor symptoms [1]. The disease is associated with a loss of antioxidants or increase in prooxidant levels and mitochondrial dysfunction. The neurotoxin 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) is known to cause a similar loss of dopaminergic neurons in the human midbrain with corresponding Parkinsonian symptoms [2]. Several animal species have also shown sensitivity to MPTP, including primates, mice, goldfish, and, most recently, zebrafish [3]. MPTP is metabolized to 1-methyl-4-phenyl pyridinium ( ) in glial cells in the brain. After release from the glia, MPP+ is transported into dopaminergic neurons via the dopamine transporter (DAT). MPP+ accumulates in the mitochondria and induce neuronal cell death via several pathways, including the inhibition of complex I activity of the respiratory chain. This contributes to both reactive oxygen species generation and nigral cell loss. [4]. The excessive production of reactive oxygen species, such as superoxide anion, hydroxyl radical and hydrogen peroxide, may either directly damage the cellular macromolecule to cause cell
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