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Protective effects of cultured and fermented ginseng extracts against scopolamine-induced memory loss in a mouse model
Author(s) -
SongHee Han,
Sung-June Kim,
Young Won Yun,
Sang-Yoon Nam,
Hu-Jang Lee,
Beom-Jun Lee
Publication year - 2018
Publication title -
laboratory animal research
Language(s) - English
Resource type - Journals
eISSN - 2233-7660
pISSN - 1738-6055
DOI - 10.5625/lar.2018.34.1.37
Subject(s) - morris water navigation task , acetylcholinesterase , ginseng , spontaneous alternation , acetylcholine , elevated plus maze , aché , hippocampus , scopolamine , pharmacology , medicine , chemistry , traditional medicine , endocrinology , biochemistry , pathology , enzyme , anxiety , alternative medicine , psychiatry
This study was performed to investigate the effect of a concentrate of fermented wild ginseng root culture (HLJG0701) on memory improvement in the scopolamine (SPL)-induced memory-deficient mouse model. Eight-week-old male ICR mice were used to evaluate the protective effect of HLJG0701 against the SPL-induced memory loss animal model. The Morris water maze test, which measures hippocampus-dependent learning ability, and the Y-maze test, a short-term memory assessment test, were performed and related markers were analyzed. HLJG0701-treated groups displayed significantly reduced acetylcholinesterase activity and increased acetylcholine level compared with the SPL-administered group (SPL-G) ( P <0.05). In the Y-maze test, the spontaneous alternation in al HLJG0711-treated groups was significantly increased compared with that in SPL-G ( P <0.05). In the Morris water maze test, the escape latency and time spent in the target quadrant in all HLJG0701-treated groups were significantly decreased and increased, respectively, compared with those in SPL-G ( P <0.05). In addition, the brain-derived neurotrophic factor level in groups treated with HLJG0701 300 and 600 mg/kg body weight was significantly increased compared with that in SPL-G ( P <0.05). These results suggest that the HLJG0701 may protect against memory loss by inhibiting acetylcholinesterase activity and preventing acetylcholine deficiency.

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