Dutch
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
Journal of Pharmacy and Pharmacology 2014-Sep

Aloysia gratissima prevents cellular damage induced by glutamatergic excitotoxicity.

Alleen geregistreerde gebruikers kunnen artikelen vertalen
Log in Schrijf in
De link wordt op het klembord opgeslagen
Ana L B Zeni
Samuel Vandresen-Filho
Tharine Dal-Cim
Wagner C Martins
Daniela B Bertoldo
Marcelo Maraschin
Carla I Tasca

Sleutelwoorden

Abstract

OBJECTIVE

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.

RESULTS

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.

Word lid van onze
facebookpagina

De meest complete database met geneeskrachtige kruiden, ondersteund door de wetenschap

  • Werkt in 55 talen
  • Kruidengeneesmiddelen gesteund door de wetenschap
  • Kruidenherkenning door beeld
  • Interactieve GPS-kaart - tag kruiden op locatie (binnenkort beschikbaar)
  • Lees wetenschappelijke publicaties met betrekking tot uw zoekopdracht
  • Zoek medicinale kruiden op hun effecten
  • Organiseer uw interesses en blijf op de hoogte van nieuwsonderzoek, klinische onderzoeken en patenten

Typ een symptoom of een ziekte en lees over kruiden die kunnen helpen, typ een kruid en zie ziekten en symptomen waartegen het wordt gebruikt.
* Alle informatie is gebaseerd op gepubliceerd wetenschappelijk onderzoek

Google Play badgeApp Store badge