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Neuroprotective effect of peanut sprout extract and its solvent soluble fractions on glutathione‐depleted neuronal HT22 cells (629.11)
Author(s) -
Kim Seong Soon
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.629.11
Subject(s) - glutathione , neuroprotection , glutathione reductase , chemistry , oxidative stress , buthionine sulfoximine , antioxidant , biochemistry , pharmacology , glutamate receptor , glutathione peroxidase , enzyme , biology , receptor
Neuroprotective Effect of Peanut Sprout Extract and Its Solvent Soluble Fractions on Glutathione‐Depleted Neuronal HT22 cells Brain is vulnerable to oxidative stress more than other organs, because it consumes about 20% of oxygen in the body and contains much polyunsaturated fatty acid. As oxidative stress is associated with many neurodegenerative disorders, it is clinically essential to screen neuroprotective agents. In this context, we investigated that the neuroprotective effect of peanut sprout extract (PSE) and its hexane ‐ , methylene chloride ‐ soluble fractions on glutathione‐depleted mouse hippocampal HT22 cells in the presence of glutamate, buthionine sulfoximine (BSO, a specific inhibitor of gamma‐glutamate cysteine ligase (GCL)) and 1,3‐bis(2‐chloroethyl)‐1‐nitrourea (BCNU, as a specific inhibitor of glutathione reductase (GR)) known as inducers of homeostatic imbalance of glutathione. The protective effect of PSE and solvent soluble fractions were evaluated by oxytosis and H 2 DCFDA assays in the HT22 cells under the homeostatic imbalance with glutathione. The results showed that PSE and its fractions significantly increased the cell viability under GSH‐depleted state. While they induced some antioxidant enzyme including glutathione reductase. Thus, neuroprotective effect of PSE and its solvent fraction appears to be mediated by their potential to increase the expression of antioxidant enzyme rather than directly scavenging ROS. However, the protective mechanism of action needs to be further studied.