Remote Ischemia Preconditioning Attenuates Blood-Spinal Cord Barrier Breakdown in Rats Undergoing Spinal Cord Ischemia Reperfusion Injury: Associated with Activation and Upregulation of CB1 and CB2 Receptors.
Cell Physiol Biochem
; 43(6): 2516-2524, 2017.
Article
em En
| MEDLINE
| ID: mdl-29130941
ABSTRACT
BACKGROUND/AIMS:
Remote ischemic preconditioning (RIPC) has protective effects on spinal cord ischemia reperfusion (I/R) injury, but the potential mechanisms remain unclear. In our study, the effects and underlying mechanisms of RIPC on blood-spinal cord barrier (BSCB) breakdown following I/R injury were investigated.METHODS:
animals underwent intraperitoneal administration with cannabinoid-1 (CB1) receptor antagonist AM251, cannabinoid-2 (CB2) receptor antagonist AM630 or vehicle 15 minutes before three 3-minute occlusion-reperfusion cycles on the right femoral artery or a sham operation. 30 minutes after the preconditioning, aortic arch was exposed with or without 14-minute occlusion. Neurological function was assessed with Tarlov scoring system. The disruption of BSCB was assessed by measuring Evans Blue (EB) extravasation. The expression of tight junction protein occludin was determined by western blot analyses. The expression and localization of CB1 and CB2 receptors were assessed by western blot and immunofluorescence.RESULTS:
RIPC attenuated the motor dysfunction, BSCB disruption and downregulation of occludin after I/R injury, which were impaired by blocking CB1 and CB2 receptors. Moreover, RIPC upregulated the elevated perivascular expression of CB1 and CB2 receptors following I/R injury.CONCLUSIONS:
These results indicated that RIPC, through activation and upregulation of CB1 and CB2 receptors, was involved in preserving the integrity of BSCB after spinal cord I/R injury.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Medula Espinal
/
Traumatismo por Reperfusão
/
Precondicionamento Isquêmico
/
Receptor CB1 de Canabinoide
/
Receptor CB2 de Canabinoide
Tipo de estudo:
Prognostic_studies
/
Risk_factors_studies
Limite:
Animals
Idioma:
En
Revista:
Cell Physiol Biochem
Ano de publicação:
2017
Tipo de documento:
Article