Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity
| Autor: | Carla I. Tasca, Tharine Dal-Cim, Samuel Vandresen-Filho, Wagner C. Martins, Ana Lúcia Bertarello Zeni, Marcelo Maraschin, Daniela Bohn Bertoldo |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Coumaric Acids Cell Survival Excitatory Amino Acids Excitotoxicity Glutamic Acid Pharmaceutical Science Mice Inbred Strains Pharmacology medicine.disease_cause Hippocampus Receptors N-Methyl-D-Aspartate Neuroprotection chemistry.chemical_compound Glutamatergic Seizures Verbenaceae Excitatory Amino Acid Agonists medicine Animals Cell damage Cell Death Plant Extracts Glutamate receptor Neurotoxicity Biological Transport Quinolinic Acid medicine.disease Neuroprotective Agents chemistry NMDA receptor Neurotoxicity Syndromes Phosphatidylinositol 3-Kinase Phytotherapy Quinolinic acid |
| Zdroj: | Journal of Pharmacy and Pharmacology. 66:1294-1302 |
| ISSN: | 2042-7158 0022-3573 |
| DOI: | 10.1111/jphp.12250 |
| Popis: | Objectives Aloysia gratissima aqueous extract (AE) was investigated as a putative protective agent against quinolinic acid (QA)-induced seizures in mice and hippocampal cell damage. Additionally, AE and ferulic acid (FA), the major compound of AE, were tested against neurotoxicity evoked by glutamate or its N-methyl-D-aspartate receptor (NMDAR) agonist, QA on hippocampal slices, in vitro. Methods Mice were treated with AE before QA infusion (36.8 nmol/site) and seizures were analysed. Cellular viability and modulation of excitatory amino acid transport were verified in hippocampal slices. In-vitro AE or FA was tested against neurotoxicity induced by glutamate or QA. Key findings AE did not prevent QA-induced seizures; however, it prevented cellular death and disruption of excitatory amino acid transport. In-vitro AE (0.1 or 1.0 mg/ml) or FA (1 or 10 μm), improved cell viability against citotoxicity exerted by glutamate or QA, respectively. Both AE and FA have protective effects depending on activation of the phosphatidylinositol-3 kinase (PI3K) signalling pathway. Conclusions AE attenuated QA-induced cell damage possibly involving the glutamate transport modulation through NMDAR interaction. FA shows a similar profile of neuroprotection promoted by AE. Therefore, AE treatment might be a useful strategy in preventing brain damage caused by exacerbation of glutamatergic toxicity in nervous system disorders. |
| Databáze: | OpenAIRE |
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