Effects of intracerebroventricular injection of delta-opioid receptor agonist TAN-67 or antagonist naltrindole on acute cerebral ischemia in rat.
- Author:
Xue-Song TIAN
1
;
Fei ZHOU
;
Ru YANG
;
Ying XIA
;
Gen-Cheng WU
;
Jing-Chun GUO
Author Information
1. National Key Laboratory of Medical Neurobiology, Department of Integrative Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain;
pathology;
Brain Ischemia;
drug therapy;
Infarction, Middle Cerebral Artery;
Injections, Intraventricular;
Naltrexone;
analogs & derivatives;
pharmacology;
Quinolines;
pharmacology;
Rats;
Rats, Sprague-Dawley;
Receptors, Opioid, delta;
agonists;
Reperfusion Injury
- From:
Acta Physiologica Sinica
2008;60(4):475-484
- CountryChina
- Language:Chinese
-
Abstract:
This work was performed to determine the role of delta-opioid receptor (DOR) in protection against acute ischemia/reperfusion injury. Transient (1 h) focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). DOR agonist TAN-67 (30 nmol, 60 nmol, 200 nmol), DOR antagonist naltrindole (20 nmol, 50 nmol, 100 nmol) or artificial cerebral spinal fluid (aCSF) was injected respectively into the lateral cerebroventricle of the rat 30 min before the induction of brain ischemia. Neurological deficits were assessed by the five-grade system (Longa's methods). The brain infarct was measured by cresyl violet (CV) staining and infarct volume was analyzed by an image processing and analysis system. The expression of DOR was detected by Western blot. The results showed that 60 nmol TAN-67 significantly reduced the infarct volume (P<0.05), attenuated neurological deficits (P<0.05) and tended to increase the expression of about 60 kDa DOR protein (P>0.05), while 100 nmol naltrindole aggravated ischemic damage and decreased about 60 kDa DOR protein expression (P<0.05). These results suggest that DOR activation protects the brain against acute ischemia/reperfusion injury in rat.
