Protective effect of Gastrodia elata blume extracts on cerebral injury induced by middle cerebral artery occlusion in rats

Stroke is one of leading cause of death and long-lasting disability. Ischemia-reperfusion (IR) is very initial events of ischemic stroke and leads to neuronal damage. Gastrodia elata blume (GEB) is an herb traditionally used for the treatment of cerebrovascular related diseases in Korea. In this study, we investigated the effects of aqueous extracts of GEB and 4-hydroxylbenzyl alcohol (HBA), an active ingredient of GEB, on focal cerebral IR injury induced by middle cerebral artery occlusion (MCAO) for 2h followed by reperfusion for 24h or 72h. Male SD rats were randomly divided into 4 groups: Sham group; IR group; GEB-treated group (24 mg/kg); and HBA-treated group. Animals were administered with distilled water (Sham and IR group), GEB or HBA for 28 days. One day after last treatment, all animals were underwent MCAO and sacrificed at 24 or 72 hr after reperfusion. The recoveries of neurological function were estimated by behavioral tests, neurological defect scoring and 2,3,5-triphenyltetrazolium chloride staining. Serum malondialdehyde (MDA) and superoxide dismutase (SOD) were assayed by colorimetry. Histological structures were observed by hematoxylin and eosin staining. Immunohistochemistry was performed to detect the TNF-α, IL-6 and apoptosis. Behavior tests showed that GEB or HBA-treated groups got better scores than IR group. GEB or HBA administration significantly reduced the neurological defect scores and lessened the cerebral infarction volume. The treatment of GEB or HBA lowered MDA content and up-regulated SOD levels. Histological examination indicated that dense neuropil and more surviving neurons were seen in GEB- or HBA-treated rats. GEB or HBA administration decreased TNF-α, IL-6 and TUNEL positive cells significantly. The results suggest that GEB or HBA demonstrates a strong and ameliorative effect on cerebral IR damage and its mechanisms are associated with its properties of anti-apoptosis and anti-oxidation.