Abstract
Glutamate is a major endogenous excitatory neurotransmitter in the brain and contributes to the development of neurodegenerative diseases by excessive activation. The purpose of the present study was to determine the neuroprotective effect of Sapindus laurifolia (MESL) Fraction A against glutamate-induced oxidative stress and to assess the underlying mechanism. MESL Fraction A was subjected to a neuroprotective effect assay in HT22 mouse hippocampal cells. The mechanism underlying the neuroprotective effect of MESL Fraction A was evaluated by assaying Reactive Oxygen Species (ROS) levels, intracellular Ca2+ levels, mitochondrial membrane potential and glutathione level and antioxidant enzyme activity in HT22 cells. MESL Fraction A significantly decreased glutamate-induced death of HT22 cells (88.23 ± 1.65% relative neuroprotection). MESL Fraction A reduced the intracellular ROS and Ca2+ levels and increased the glutathione level and glutathione reductase and glutathione peroxide activities. Moreover, MESL Fraction A attenuated the mitochondrial membrane potential in HT22 cells. These results suggested that MESL Fraction A exerts a neuroprotective effect against oxidative stress HT22 cells, which was mediated by its antioxidant activity.
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