Neuroprotective Action of Deer Bone Extract Against Glutamate or Aβ1-42-Induced Oxidative Stress in Mouse Hippocampal Cells

被引:10
作者
Kim, Cho Rong [1 ]
Jeon, Hye Lyun [1 ]
Shin, Suk Kyung [1 ]
Kim, Hyun Jeong [1 ]
Ahn, Chang-Won [2 ]
Jung, Sung Ug [2 ]
Park, Soo-Hyun [2 ]
Kim, Mee Ree [1 ]
机构
[1] Chungnam Natl Univ, Dept Food & Nutr, Daejon 305764, South Korea
[2] Nong Shim Co Ltd, Res & Dev Ctr, Seoul, South Korea
关键词
A(1-42); deer bone extract; glutamate; HT-22; cells; oxidative stress; neuroprotection; PROTECTS NERVE-CELLS; HT-22; CELLS; NEURODEGENERATIVE DISORDERS; PREVENT GLUTAMATE; SIALIC-ACID; DEATH; GANGLIOSIDES; TOXICITY; ANTLER; GLUTATHIONE;
D O I
10.1089/jmf.2013.2951
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Water extracts of deer bone, called nokgol in Korean, and deer antlers have been traditionally used as anti-aging medicines. Deer antler extract is known to possess various activities, including anti-aging or anti-amnesic activitiy. However, there are no reports about the neuroprotective effect of deer bone extract (DBE). The objective of this study was to examine the neuroprotective effect of DBE on glutamate-induced cell death of mouse hippocampal cells (HT-22 cells) and to elucidate the mode of neuroprotective action of DBE. In this study, HT-22 cells was pretreated with DBE before stimulation with glutamate, and then, the effects of DBE on cell viability, oxidative stress markers, and MAP kinases were determined. Separately, the effect of DBE on H2O2 or amyloid beta peptide (1-42) (A(1-42))-induced cytotoxicity of HT-22 cells was evaluated. DBE protected HT-22 cells from glutamate-induced cell death and prevented the increase in lactate dehydrogenase leakage in HT-22 cells. DBE also prevented glutamate-induced oxidative stress, as indicated by increased reactive oxygen species and lipid peroxidation as well as by decreases in glutathione (GSH) levels and GSH peroxidase activity. In addition, DBE inhibited glutamate-induced activation of c-Jun N-terminal kinases (JNK), p38, and extracellular signal-regulated kinase, indicators of oxidative stress-induced cell death. Furthermore, DBE also protected against H2O2 and A(1-42)-induced cytotoxicity. These results suggest that DBE may be a useful functional agent for the prevention against neurodegenerative disorders involving oxidative stress.
引用
收藏
页码:226 / 235
页数:10
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