Aquilariae Lignum extract attenuates glutamate-induced neuroexcitotoxicity in HT22 hippocampal cells
| Autor: | Won-Yong Kim, Samkeun Lee, Chang-Gue Son, Yoo-Jin Jeon, Jin-Seok Lee |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Programmed cell death Time Factors Excitotoxicity Glutamic Acid Apoptosis medicine.disease_cause Neuroprotection Hippocampus Cell Line 03 medical and health sciences Mice 0302 clinical medicine medicine Excitatory Amino Acid Agonists Animals Viability assay Calcium Signaling Pharmacology Neurons Plants Medicinal biology Dose-Response Relationship Drug Chemistry Calpain Plant Extracts Glutamate receptor General Medicine Cell biology 030104 developmental biology Neuroprotective Agents Thymelaeaceae biology.protein Apoptotic signaling pathway Reactive Oxygen Species Excitatory Amino Acid Antagonists 030217 neurology & neurosurgery Phytotherapy |
| Zdroj: | Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 106 |
| ISSN: | 1950-6007 |
| Popis: | 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 μg/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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect