Abstract
BackgroundGlutamate (an endogenous excitatory neurotransmitter) at high concentrations contributes to the development of neurodegenerative diseases. Aronia melanocarpa (A. melanocarpa) berries contain anthocyanins and have high antioxidant activities. In this study, we evaluated whether A. melanocarpa berries could protect neuronal cells against glutamate-induced oxidative stress.MethodA. melanocarpa berries exerted a protective effect against cytotoxicity in HT22 mouse hippocampal cells by MTT assay. We evaluated oxidative stress parameters including ROS level, intracellular Ca2+ level, glutathione level and antioxidant enzyme activity in HT22 cells to elucidate the mechanism of its neuroprotective effect.ResultsA. melanocarpa berries decreased glutamate-induced death of HT22 cells. In addition, A. melanocarpa berries reduced ROS and intracellular Ca2+ levels. Glutathione level, antioxidant enzymes, glutathione reductase and glutathione peroxide activities and mitochondrial membrane potential were also increased in HT22 cells.ConclusionThese results suggested that A. melanocarpa berries protected HT22 cells by exerting an antioxidant effect.
Highlights
Glutamate at high concentrations contributes to the development of neurodegenerative diseases
Glutathione level, antioxidant enzymes, glutathione reductase and glutathione peroxide activities and mitochondrial membrane potential were increased in HT22 cells
These results suggested that A. melanocarpa berries protected HT22 cells by exerting an antioxidant effect
Summary
Glutamate (an endogenous excitatory neurotransmitter) at high concentrations contributes to the development of neurodegenerative diseases. We evaluated whether A. melanocarpa berries could protect neuronal cells against glutamate-induced oxidative stress. Neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease and Huntington’s disease are characterized by loss of neuronal function and memory and cognitive impairment [1]. Oxidative stress, including lipid peroxidation, free radical formation, protein oxidation and DNA oxidation, in the central nervous system (CNS) can lead to cell death and contributes to the pathogenesis of various neurodegenerative disorders [3, 4]. Glutamate is an excitatory neurotransmitter that plays a role in learning and memory, and contributes to excitotoxicity in neuronal cells [5]. Glutamate excitotoxicity results in mitochondrial dysfunction and depletion of antioxidant defense systems, including glutathione (GSH), glutathione peroxidase (GPx) and glutathione reductase (GR) by inhibiting cystine uptake [7,8,9]
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