Ethanol Extract from Asparagus Cochinchinensis Attenuates Glutamate-Induced Oxidative Toxicity in HT22 Hippocampal Cells

Abstract

We investigated the neuroprotective effect of an ethanol extract from Asparagus cochinchinensis (AC) against glutamate-induced toxicity in the HT22 hippocampal cell, which is an ideal in vitro model for oxidative stress. The neuroprotective effects of AC in HT22 cells were evaluated by analyzing cell viability, lactate dehydrogenase (LDH), flow cytometry for cell death types, reactive oxygen species (ROS), mitochondria membrane potential (MMP), and Western blot assays. In the cell death analysis, AC treatment resulted in significantly attenuated glutamate-induced loss of cell viability with a decrease in LDH release. AC treatment also reduced glutamate-induced apoptotic cell death. In the ROS and MMP analysis, AC treatment inhibited the elevation of intracellular ROS induced by glutamate exposure and the disruption of MMP. In oxidative stress-related proteins analysis, AC treatment inhibited the expression of poly ADP ribose polymerase and heme oxygenase-1 by glutamate. These results indicate that AC exerts a significant neuroprotective effect against glutamate-induced hippocampal damage by decreasing ROS production and stabilizing MMP. Thus, AC potentially provides a new strategy for the treatment of oxidative stress-related diseases.

Sargachromenol Isolated from Sargassum horneri Attenuates Glutamate-Induced Neuronal Cell Death and Oxidative Stress through Inhibition of MAPK/NF-κB and Activation of Nrf2/HO-1 Signaling Pathway

“…The well-known pathways are mediated by the glutamate receptor N-methyl-D-aspartate (NMDA), which leads to an excessive influx of Ca 2+ , resulting in the activation of calpain and other proteases that mediate cytoskeletal damage, accompanied by mitochondrially derived reactive oxygen species (ROS) and subsequent neuronal cell death [6][7][8]. Another pathway is the inhibition of the influx of the amino acid cystine through the glutamate/cystine antiporter without passing through the glutamate receptor, and reducing the concentration of glutathione, the precursor of cystine in the cell, which increases ROS production, leading to cell death [9,10]. Both mechanisms induce apoptosis by the overexpression of ROS.…”