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KMID : 0616120180490030231
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Korean Journal of Pharmacognosy
2018 Volume.49 No. 3 p.231 ~ p.239
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Protective Effects of Hyperoside from Juglans sinensis Leaves against 1-methyl-4-phenylpyridinium-Induced Neurotoxicity
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Pariyar Ramesh
Svay Thida
Seo Jung-Won
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Abstract
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Parkinson’s disease (PD), one of common neurodegenerative diseases, is caused by the death of dopaminergic neurons in the substantia nigra pars compacta. The loss of dopaminergic neurons in PD is associated with oxidative stress and mitochondrial dysfunction. Hyperoside (quercetin 3-O-β-D-galactopyranoside) was reported to have protective properties against oxidative stress by reducing intracellular reactive oxygen species (ROS) and increasing antioxidant enzyme activity. In this study, we examined the neuroprotective effect of hyperoside against 1-methyl-4-phenyl pyridinium (MPP+)-induced cell model of PD and the underlying molecular mechanisms. Hyperoside significantly decreased MPP+-induced cell death, accompanied by a reduction in poly ADP-ribose polymerase (PARP) cleavage. Furthermore, it attenuated MPP+-induced intracellular ROS and disruption of mitochondrial membrane potential (MMP), with the reduction of Bax/Bcl-2 ratio. Moreover, hyperoside significantly increased the phosphorylation of Akt, but it has no effects on GSK3β and MAPKs. Pharmacological inhibitor of PI3K/Akt abolished the cytoprotective effects of hyperoside against MPP+. Taken together, these results demonstrate that hyperoside significantly attenuates MPP+-induced neurotoxicity through PI3K/Akt signaling pathways in SH-SY5Y cells. Our findings suggest that hyperoside might be one of the potential candidates for the treatment of PD.
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KEYWORD
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Hyperoside, Parkinson’s disease, MPP+, Neurotoxicity, ROS, Akt
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