Geniposide attenuates postischemic long-term potentiation via GluN2A.
Pak J Pharm Sci
; 34(3): 909-914, 2021 May.
Article
en En
| MEDLINE
| ID: mdl-34602413
ABSTRACT
N-Methyl-D-aspartate receptor (NMDAR)-induced antioxidation is a significant cause of neuronal injury after ischemic stroke. In a previous work, we verified the neuroprotective roles of geniposide during tMCAO in vivo. However, it remains unknown whether geniposide ameliorates injury to hippocampal neurons during Ischemic Long Term Potentiation (iLTP) induction in vitro. After induction of cells oxygen-glucose deprivation or hydrogen peroxide, the protection of geniposide evaluated by MTT assay and electrophysiological tests. In this study, we suggested neuronal cell apoptosis was attenuated by geniposide. Furthermore, field excitatory postsynaptic potentials (fEPSCs) following postischemic LTP were assessed by electrophysiological tests. Finally, we determined that medium and high doses of geniposide attenuated oxidative stress insult and improved iLTP. Importantly, these effects were abolished by cotreatment with geniposide and the GluN2A antagonist NVP. In contrast, the GluN2B inhibitor ifenprodil failed to have an effect. In conclusion, we suggest for the first time that treatment with geniposide can attenuate postischemic LTP induction in a concentration-dependent manner. We infer that GluN2A-containing NMDARs are involved in the neuroprotection induced by geniposide treatment in ischemia.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Receptores de N-Metil-D-Aspartato
/
Potenciación a Largo Plazo
/
Potenciales Postsinápticos Excitadores
/
Hipoxia-Isquemia Encefálica
/
Iridoides
/
Neuronas
Límite:
Animals
Idioma:
En
Revista:
Pak J Pharm Sci
Asunto de la revista:
FARMACIA
/
FARMACOLOGIA
/
QUIMICA
Año:
2021
Tipo del documento:
Article
País de afiliación:
China