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Sci Rep. 2015 May 14;5:9651. doi: 10.1038/srep09651.

Hippocampal memory enhancing activity of pine needle extract against scopolamine-induced amnesia in a mouse model.

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Liver and Immunology Research Center, Oriental Medical College of Daejeon University, 22-5 Daehung-dong, Jung-gu, Daejeon, 301-724, Republic of Korea.
TKM-based Herbal Drug Research Group, Korea Institute of Oriental Medicine, Daejeon 305-811, Republic of Korea.
Department of Applied Chemistry, Oriental Medicine College of Daejeon University, 62, Daehak-ro, Dong-gu, Daejeon, 300-716, Republic of Korea.
Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, Republic of Korea.


We evaluated the neuropharmacological effects of 30% ethanolic pine needle extract (PNE) on memory impairment caused by scopolamine injection in mice hippocampus. Mice were orally pretreated with PNE (25, 50, and 100 mg/kg) or tacrine (10 mg/kg) for 7 days, and scopolamine (2 mg/kg) was injected intraperitoneally, 30 min before the Morris water maze task on first day. To evaluate memory function, the Morris water maze task was performed for 5 days consecutively. Scopolamine increased the escape latency and cumulative path-length but decreases the time spent in target quadrant, which were ameliorated by pretreatment with PNE. Oxidant-antioxidant balance, acetylcholinesterase activity, neurogenesis and their connecting pathway were abnormally altered by scopolamine in hippocampus and/or sera, while those alterations were recovered by pretreatment with PNE. As lipid peroxidation, 4HNE-positive stained cells were ameliorated in hippocampus pretreated with PNE. Pretreatment with PNE increased the proliferating cells and immature neurons against hippocampal neurogenesis suppressed by scopolamine, which was confirmed by ki67- and DCX-positive stained cells. The expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element-binding protein (pCREB) in both protein and gene were facilitated by PNE pretreatment. These findings suggest that PNE could be a potent neuropharmacological drug against amnesia, and its possible mechanism might be modulating cholinergic activity via CREB-BDNF pathway.

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