The effects of gabapentin pretreatment on brain injury induced by focal cerebral ischemia/reperfusion in the rat.
10.4097/kjae.2010.58.2.184
- Author:
Yoo Kyung KIM
1
;
Jeong Gill LEEM
;
Ji Yeon SIM
;
Sung Moon JEONG
;
Kyoung Woon JOUNG
Author Information
1. Department of Anesthesiology and Pain Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. jgleem@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Caspase-3;
Focal cerebral ischemia/reperfusion;
Gabapentin;
Heat shock protein 70;
Rat
- MeSH:
Administration, Intravenous;
Amines;
Animals;
Apoptosis;
Brain;
Brain Edema;
Brain Injuries;
Brain Ischemia;
Caspase 3;
Cyclohexanecarboxylic Acids;
gamma-Aminobutyric Acid;
HSP70 Heat-Shock Proteins;
Humans;
Infarction;
Infarction, Middle Cerebral Artery;
Male;
Neurons;
Neuroprotective Agents;
Rats;
Rats, Sprague-Dawley
- From:Korean Journal of Anesthesiology
2010;58(2):184-190
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Experimental studies have shown that gabapentin can reduce neuronal injury in the setting of cerebral ischemia, but the mechanisms have not yet been clearly determined. This study was conducted to determine whether gabapentin pretreatment altered expression levels of heat shock protein 70 and reduced acute phase neuronal injury in rats subjected to transient focal cerebral ischemia/reperfusion. METHODS: Forty male Sprague-Dawley rats (260-300 g) were randomly assigned to one of four groups (saline-treated, or 0.1, 0.5, or 5 mg/kg gabapentin group). In all animals, focal cerebral ischemia was induced by intraluminal middle cerebral artery occlusion for 1 hour. The animals of the gabapentin groups were pretreated with a single intravenous administration of gabapentin 20 minutes before ischemic insults. The infarct volume, brain edema and motor behavior deficits were analyzed 24 hours after ischemic insult. Caspase-3-reactive cells and cells showing Hsp70 activity were counted in the caudoputamen and fronto-parietal cortex. RESULTS: The infarction ratio was significantly decreased in the 5 mg/kg gabapentin group (P < 0.05) and brain edema ratios were significantly reduced in the 0.1 mg/kg, 0.5 mg/kg, and 5 mg/kg gabapentin groups 24 hours after ischemia/reperfusion injury (P < 0.05). There were more Hsp70-reactive cells in the 5 mg/kg gabapentin group than in the saline group in both the caudoputamen and fronto-parietal cortex (P < 0.05). CONCLUSIONS: These results indicate that gabapentin may have a neuroprotective effect and can reduce early neuronal injury caused by focal cerebral ischemia/reperfusion; this may be mediated by expression of Hsp70. However, gabapentin pretreatment did not prevent caspase-dependent apoptosis.
