Journal
NEUROCHEMICAL RESEARCH
Volume 42, Issue 5, Pages 1299-1307Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-016-2171-y
Keywords
Ginsenoside Rg1; Lipopolysaccharide; Cognitive impairment; Acetylcholine; Alpha7 nicotinic acetylcholine receptor
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Funding
- Provincial Natural Science Foundation of Shandong [ZR2015HQ002]
- National Natural Science Foundation of China [81572534, 81602226]
- Provincial Projects of Medical and Technology Development Program of Shandong [2014WS0091, 2014WS0347]
- Key Research and Development Program of Shandong Province [2015GSF118096]
- China Postdoctoral Science Foundation [2016M590641]
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Bacterial endotoxin lipopolysaccharide (LPS) can induce systemic inflammation, and therefore disrupt learning and memory processes. Ginsenoside Rg1, a major bioactive component of ginseng, is shown to greatly improve cognitive function. The present study was designed to further investigate whether administration of ginsenoside Rg1 can ameliorate LPS-induced cognitive impairment in the Y-maze and Morris water maze (MWM) task, and to explore the underlying mechanisms. Results showed that exposure to LPS (500 mu g/kg) significantly impaired working and spatial memory and that repeated treatment with ginsenoside Rg1 (200 mg/kg/day, for 30 days) could effectively alleviate the LPS-induced cognitive decline as indicated by increased working and spatial memory in the Y-maze and MWM tests. Furthermore, ginsenoside Rg1 treatment prevented LPS-induced decrease of acetylcholine (ACh) levels and increase of acetylcholinesterase (AChE) activity. Ginsenoside Rg1 treatment also reverted the decrease of alpha7 nicotinic acetylcholine receptor (alpha 7 nAChR) protein expression in the prefrontal cortex (PFC) and hippocampus of LPS-treated rats. These findings suggest that ginsenoside Rg1 has protective effect against LPS-induced cognitive deficit and that prevention of LPS-induced changes in cholinergic system is crucial to this ameliorating effect.
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