Effects of piperphentonamine hydrochloride on cognitive deficits in rats induced by cerebral ischemia-reperfusion.
- Author:
Han-yi ZHU
1
;
Juan BIN
;
Chuang WANG
;
Huan-bing LIN
;
Heng ZHOU
;
Jiang-ping XU
Author Information
- Publication Type:Journal Article
- MeSH: 3,4-Methylenedioxyamphetamine; analogs & derivatives; therapeutic use; Animals; Brain Ischemia; drug therapy; Cognition Disorders; prevention & control; Infarction, Middle Cerebral Artery; drug therapy; Male; Neuroprotective Agents; therapeutic use; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; drug therapy; prevention & control
- From: Journal of Southern Medical University 2011;31(11):1858-1862
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of piperphentonamine hydrochloride (PPTA) on cognitive deficits induced by ischemia-reperfusion and explore the possible mechanisms.
METHODSSD rats were randomly divided into sham-operated group, ischemia-reperfusion group (with saline injection), PPTA-treated groups (2.5, 5, 10 mg/kg) and edaravone-treated group (6 mg/kg). Cerebral ischemia-reperfusion injury was induced by middle cerebral artery occlusion, and the agents were administrated 1 h after ischemia. At 24 h after ischemia, step-through passive avoidance test was carried out, and 24 h later IL-1β, TNF-α, caspase-3 and HSP-70 mRNA expressions in the ischemic brain tissues were measured with RT-PCR.
RESULTSIn the step-through passive avoidance test, the rats in the ischemia-reperfusion group showed significantly shorter latency and more error times than those in the sham group, and these behavioral changes were improved significantly by treatments with PPTA and edaravone. Cerebral ischemia-reperfusion caused significantly increased expressions of IL-1β, TNF-α, caspase-3 and HSP-70 mRNA, and these changes were obviously reversed by PPTA, but not by edaravone.
CONCLUSIONSPPTA can reverse cognitive deficits induced by cerebral ischemia-reperfusion probably by decreasing the inflammatory responses and cell apoptosis in the brain, suggesting its potential as a new therapeutic agent for improving the cognitive function following cerebral ischemia-reperfusion.