Abstract
Oxidative stress plays an important role in Parkinson’s disease and other neurodegenerative disorders. Lycium barbarum polysaccharides (LBP), the main active ingredients extracted from the fruits of Lycium barbarum L., have been shown to be a potent antioxidant. In the present study, we investigated the protective effects, and the possible mechanism of action of LBP against 6-hydroxydopamine (6-OHDA)-induced apoptosis in PC12 cells. Our data demonstrated that LBP significantly reversed the 6-OHDA-induced decrease in cell viability, prevented 6-OHDA-induced changes in condensed nuclei and decreased the percentage of apoptotic cells in a dose-dependent manner. Furthermore, LBP also slowed the accumulation of reactive oxygen species (ROS) and nitric oxide (NO), decreased the level of protein-bound 3-nitrotyrosine (3-NT) and intracellular free Ca2+, and inhibiting the overexpression of nuclear factor κB (NF-κB), neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS). These results demonstrate that LBP prevents 6-OHDA-induced apoptosis in PC12 cells, at least in part through the ROS-NO pathway.
Highlights
Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease (AD), is mainly characterized by pathological irreversible loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc) [1,2]
To determine whether Lycium barbarum polysaccharides (LBP) alone had any effects on cell viability, PC12 cells treated with various concentrations of LBP for 24 h
Cells treated with various concentrations of LBP for 24 h before the addition of 6-OHDA (75 μM) for 24 h showed that cell viability increased at concentrations of LBP
Summary
Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease (AD), is mainly characterized by pathological irreversible loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc) [1,2]. Current data indicates that oxidative damage represents a final common pathway in the pathogenesis of PD-like disorders [4,5,6], suggesting that compounds interfering with production of reactive oxygen species (ROS) and nitric oxide (NO) or with impairment of mitochondrial activity might be protective [7]. Several lines of evidence in PD patients and animal models have suggested that oxygen-free radicals and oxidative stress are involved in the pathogenesis of PD [8,9,10]. Medicinal herbs that have antioxidative effects are being considered as therapeutic agents against neuronal loss [7,11,12]
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