Abstract
The aim of the present study was to examine the protective effect of γ-mangostin, a component of the mangosteen shell, against oxidative damage to nerve cells induced by excessive glutamate, a known excitatory neurotransmitter. To investigate the effect of γ-mangostin on apoptosis, 5 mM of glutamate was used to induce apoptotic cell death in mouse hippocampal HT22 cells. In this study, γ-mangostin was found to exert a stronger protection than N-acetyl cysteine against glutamate-induced cell damage. γ-Mangostin showed prevented glutamate-induced apoptosis in HT22 cells by reducing the production of reactive oxygen species and stimulating the expression of heme oxygenase-1 protein. In addition, glutamate significantly induced the accumulation of intracellular calcium ions, whereas treatment with γ-mangostin markedly reduced it. Hoechst 33342 staining showed an improvement in glutamate-induced nuclear condensation following γ-mangostin treatment. Furthermore, the number of annexin V-positive cells was significantly reduced following treatment with γ-mangostin. Western blot analysis showed the inhibition of glutamate-induced mitogen-activated protein kinase phosphorylation by γ-mangostin. γ-mangostin also inhibited the regulation of the intrinsic mitochondrial apoptotic pathway. Thus, the results of this study suggest that γ-mangostin is an active ingredient of mangosteen and exerts neuroprotective activities in HT22 cells.
Highlights
There has been a growing interest in the prevention of neurodegenerative diseases owing to the steady increase in the elderly population
To determine the effect of γ-mangostin on HT22 neuronal cell apoptosis induced by 5 mM glutamate, HT22 cells in culture were treated with various concentrations of γ-mangostin (3.1, 6.2, and 12.5 μM) for 24 h
Compared to the glutamatetreated group of 25.76 ± 0.43%, the cell viability that was reduced by glutamate was significantly increased to 101.28 ± 1.71, 100 ± 1.35, and 91.68 ± 1.02% in the group treated with γ-mangostin and glutamate (Figure 1B)
Summary
There has been a growing interest in the prevention of neurodegenerative diseases owing to the steady increase in the elderly population. Neuronal cell death is a causative factor of neurodegenerative disease [2,3], and in vitro and in vivo studies have contributed to our understanding of the mechanism of neuronal cell death [4]. Glutamate works as synaptic plasticity that is capable of continuous changes in structure and function depending on the degree of activity in the brain, which is related to cognitive functions such as learning and memory [5]. If it is over-activated, it causes epilepsy and excitotoxicity as it acts as a neurotoxin [6].
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