Prolonged oral administration of Gastrodia elata extract improves spatial learning and memory of scopolamine-treated rats.
- Author:
Young Mi PARK
1
;
Bong Gun LEE
;
Sang Hoon PARK
;
Hong Geun OH
;
Yang Gyu KANG
;
Ok Jin KIM
;
Lee Seong KWON
;
Yong Phill KIM
;
Min Hyu CHOI
;
Yong Seob JEONG
;
Jisun OH
;
Hak Yong LEE
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: Gastrodia elata; scopolamine-induced memory impairment; amyloid-beta peptide; neuroprotective effect; cognitive-enhancing effect
- MeSH: Administration, Oral*; Alzheimer Disease; Animals; Body Weight; Cell Death; Gastrodia*; Learning*; Memory Disorders; Memory*; Models, Animal; Neurodegenerative Diseases; Neurons; Neuroprotective Agents; PC12 Cells; Rats*; Rats, Sprague-Dawley; Scopolamine Hydrobromide
- From:Laboratory Animal Research 2015;31(2):69-77
- CountryRepublic of Korea
- Language:English
- Abstract: Gastrodia elata (GE) is traditionally used for treatment of various disorders including neurodegenerative diseases such as Alzheimer's disease. To investigate the neuroprotective effect of GE, amyloid-beta peptide (Abeta)-treated PC12 cells were cultured with GE aqueous extract. In vitro assay demonstrated that 50 microM of pre-aggregated Abeta was lethal to about a half portion of PC12 cells and that Abeta aggregate-induced cell death was significantly decreased with GE treatment at < or =10 mg/mL in a dose-dependent manner. To further examine in vivo cognitive-improving effects, an artificial amnesic animal model, scopolamine-injected Sprague-Dawley rats, were orally administered the extract for 6 weeks followed by behavioral tests (the passive avoidance test and Morris water maze test). The results showed that an acute treatment with scopolamine (1 mg/kg of body weight) effectively induced memory impairment in normal rats and that the learning and memory capability of scopolamine-treated rats improved after prolonged administration of GE extract (50, 250 and 500 mg/kg of body weight for 6 weeks). These findings suggest that a GE regimen may potentially ameliorate learning and memory deficits and/or cognitive impairments caused by neuronal cell death.
