Protective effects of sodium beta-aescin on ischemia-reperfusion injury in rat brain.
- Author:
Xia-min HU
1
;
Fan-dian ZENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain; metabolism; Brain Ischemia; metabolism; pathology; Catalase; metabolism; Escin; pharmacology; Glutathione Peroxidase; metabolism; Male; Malondialdehyde; metabolism; Neuroprotective Agents; pharmacology; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism; pathology; Sodium-Potassium-Exchanging ATPase; metabolism; Superoxide Dismutase; metabolism
- From: Acta Pharmaceutica Sinica 2004;39(6):419-423
- CountryChina
- Language:English
-
Abstract:
AIMTo investigate the protective effects of sodium beta-aescin on cerebral ischemia-reperfusion injury in rats.
METHODSRats were pretreated with sodium beta-aesein for 7 d and then subjected to cerebral ischemia-reperfusion injury induced by a middle cerebral artery occlusion (MCAO). The neurological outcome was evaluated by the Longa's method; The infarct volume was assessed by hemmatoxylin-Eosin staining and the cerebral water content was measured by dry weight method. The activities of SOD, GSH-Px, CAT, Na+ -K+ -ATPase and the MDA content were measured in the cortex and hippocampus of ischemic and non-ischemic hemisphere.
RESULTSSodium beta-aescin significantly reduced the volume of cerebral infarct and water content, and ameliorated the neurological deficit (P < 0.05). In vehicle-treated rats, the activities of SOD, GSH-Px and Na+ -K+ -ATPase in the cortex and hippocampus of ischemic hemisphere were all decreased (P < 0.01) , while the CAT activity was slightly elevated and the MDA of content was significantly increased (P < 0.01) compared with the sham-operated group. After treated with sodium beta-aescin, the effects on recovery of SOD, GSH-Px, Na+ -K+ -ATPase activities were observed (P < 0.05), and the MDA content was reduced (P < 0.05).
CONCLUSIONThese results showed that pretreatment with sodium beta-aescin can attenuate brain injury and its antioxidant activity on rats which encountered cerebral ischemia-reperfusion.