Aquilariae Lignum extract attenuates glutamate-induced neuroexcitotoxicity in HT22 hippocampal cells

被引:20
作者
Lee, Jin-Seok [1 ]
Kim, Won-Yong [1 ]
Jeon, Yoo-Jin [1 ]
Lee, Sam-Keun [2 ]
Son, Chang-Gue [1 ]
机构
[1] Daejeon Univ, Oriental Med Coll, Liver & Immunol Res Ctr, 22-5 Daehung Dong, Daejeon 301724, South Korea
[2] Daejeon Univ, Oriental Med Coll, Dept Appl Chem, 62 Daehak Ro, Daejeon 300716, South Korea
关键词
Aquilariae Lignum; Excitotoxicity; Calpain-dependent; Apoptosis; Calcium overload; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; EQUINE ESTROGENS; NEURONAL CELLS; DEATH; MECHANISMS; NEURODEGENERATION; EXCITOTOXICITY; VULNERABILITY; CONTRIBUTES;
D O I
10.1016/j.biopha.2018.07.032
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
An imbalance between excitatory and inhibitory neurotransmitters is known to induce neuronal excitotoxicity which is a major cause of neurodegenerative disorders. Excessive glutamate concentration leads to the neuronal death by increasing oxidative stress and affecting the apoptotic signaling pathway. We investigated the anti-excitotoxic effects and associated working mechanisms of 30% ethanol extract of Aquilariae Lignum (ALE) against hippocampal neuronal death by glutamate. HT22 cells were treated with glutamate (20 mM) for 24 h following pretreatment with ALE (5, 10, 25 mu g/mL). Cell viability, biochemical analysis, flow chemistry, and Western blotting assays were performed. Glutamate treatment substantially increased the intracellular level of reactive oxygen species (ROS) and Ca2+ influx into the cell, which were followed by apoptosis. ALE pretreatment, however, significantly attenuated these excitotoxicity-related features according to the results of Annexin V analysis and the lactate dehydrogenase assay, in which the calpain pathway (in a caspase 3-independent manner) may be involved. ALE pretreatment also significantly attenuated the glutamate-induced activation of both inflammation-associated molecules (extracellular signal-regulated kinase, c-Jun N-terminal kinases and p38) and death-related molecules (p53, apoptosis-inducing factor). The inactivation of brain-derived neurotrophic factor (BDNF) was restored by ALE pretreatment. Our results verified that A. Lignum has potential neuroprotective effects on glutamate-induced excitotoxicity in hippocampal neuron cells, and its underlying mechanism may involve the regulation of ROS-mediated cell death pathways.
引用
收藏
页码:1031 / 1038
页数:8
相关论文
共 40 条
[1]   Neuroinflammation, Oxidative Stress and the Pathogenesis of Alzheimer's Disease [J].
Agostinho, Paula ;
Cunha, Rodrigo A. ;
Oliveira, Catarina .
CURRENT PHARMACEUTICAL DESIGN, 2010, 16 (25) :2766-2778
[2]   Neuroprotective effect of 1-methoxyoctadecan-1-ol from Uncaria sinensis on glutamate-induced hippocampal neuronal cell death [J].
Ahn, Sung Min ;
Kim, Ha Neui ;
Kim, Yu Ri ;
Oh, Eun Young ;
Choi, Young Whan ;
Shin, Hwa Kyoung ;
Choi, Byung Tae .
JOURNAL OF ETHNOPHARMACOLOGY, 2014, 155 (01) :293-299
[3]   Molecular mechanisms of glutamate-dependent neurodegeneration in ischemia and traumatic brain injury [J].
Arundine, M ;
Tymianski, M .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2004, 61 (06) :657-668
[4]   Adult hippocampal neurogenesis: Regulation, functional implications, and contribution to disease pathology [J].
Balu, Darrick T. ;
Lucki, Irwin .
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 2009, 33 (03) :232-252
[5]   Selective neuronal vulnerability of human hippocampal CA1 neurons: lesion evolution, temporal course, and pattern of hippocampal damage in diffusion-weighted MR imaging [J].
Bartsch, Thorsten ;
Doehring, Juliane ;
Reuter, Sigrid ;
Finke, Carsten ;
Rohr, Axel ;
Brauer, Henriette ;
Deuschl, Guenther ;
Jansen, Olav .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2015, 35 (11) :1836-1845
[6]   BDNF function in adult synaptic plasticity: The synaptic consolidation hypothesis [J].
Bramham, CR ;
Messaoudi, E .
PROGRESS IN NEUROBIOLOGY, 2005, 76 (02) :99-125
[7]   Unraveling the mechanisms involved in motor neuron degeneration in ALS [J].
Bruijn, LI ;
Miller, TM ;
Cleveland, DW .
ANNUAL REVIEW OF NEUROSCIENCE, 2004, 27 :723-749
[8]  
Burd I, 2016, ADV PHARMACOL, V76, P85, DOI 10.1016/bs.apha.2016.02.003
[9]   Selective vulnerability to kainate-induced oxidative damage in different rat brain regions [J].
Candelario-Jalil, E ;
Al-Dalain, SM ;
Castillo, R ;
Martínez, G ;
Fernández, OSL .
JOURNAL OF APPLIED TOXICOLOGY, 2001, 21 (05) :403-407
[10]   Protein kinase Cδ-mediated proteasomal degradation of MAP kinase phosphatase-1 contributes to glutamate-induced neuronal cell death [J].
Choi, BH ;
Hur, EM ;
Lee, JH ;
Jun, DJ ;
Kim, KT .
JOURNAL OF CELL SCIENCE, 2006, 119 (07) :1329-1340