Abstract
Purpose Excessive glutamate amount can give oxidative stress to neuronal cells, and the accumulation of cell death can trigger the neurodegenerative disorders. In this study, we discovered the neuroprotective effect of Lysimachia christinae Hance in the mouse hippocampal HT22 cell line. Method Overnight incubated HT22 cells were pretreated with L. christinae extract dose dependently (1, 10, and 100 μg/ml). Followed by then, glutamate was treated. These treated cells were incubated several times again, and cell viability, accumulation of reactive oxygen species (ROS) and Ca2+, mitochondrial membrane potential (MMP), and glutathione-related enzyme amount were measured. Results As a result, L. christinae increases the cell viability by inhibiting the ROS and Ca2+ formation, recovering the level of MMP and enhancing the activity of glutathione production compared with only vehicle-treated groups. Conclusion These draw that L. christinae may remarkably decelerate the neurodegeneration by minimizing neuronal cell damage via oxidative stress.
Highlights
Year after year, the aging population goes on increasing rapidly, and due to the extended average life expectancy, neurodegenerative disorders become the serious conversation topic
Glutamate triggers the pathological neuronal cell death by excitotoxicity, and this presumed to be mediated by reactive oxygen species (ROS) [8,9,10,11]. e glutamate toxicity can be classified by two types: receptormediated toxicity [12] and nonreceptor-mediated toxicity [13]
Oxidative glutamate toxicity is firstly occurred by high contents of extracellular glutamate which blocks the cystine inflow to the neuronal cells via the cystine/glutamate antiporter system, and this is followed by the lack of intracellular cysteine and glutathione. e depletion of the intracellular glutathione leads to accumulation of ROS resulting in cellular injury
Summary
The aging population goes on increasing rapidly, and due to the extended average life expectancy, neurodegenerative disorders become the serious conversation topic. Alzheimer’s disease, Parkinson’s disease, Huntington disease, and dementia are the typical cases that provoked by neurodegenerative disorder [2]. Glutamate triggers the pathological neuronal cell death by excitotoxicity, and this presumed to be mediated by reactive oxygen species (ROS) [8,9,10,11]. Oxidative glutamate toxicity is firstly occurred by high contents of extracellular glutamate which blocks the cystine inflow to the neuronal cells via the cystine/glutamate antiporter system, and this is followed by the lack of intracellular cysteine and glutathione. E depletion of the intracellular glutathione leads to accumulation of ROS resulting in cellular injury. Accumulation of excess ROS brings about receptormediated cellular toxicity. It evokes the overexpression of the ionotropic Ca2+ receptor [14]. It evokes the overexpression of the ionotropic Ca2+ receptor [14]. e collapse of Ca2+
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