Abstract
We evaluated the neuropharmacological effects of Gongjin-Dan (GJD) on the memory impairment caused by scopolamine injection. BALB/c mice were orally treated with GJD (100, 200, or 400 mg/kg, daily) or tacrine (THA, 10 mg/kg) for 10 days, and scopolamine (2 mg/kg) was injected intraperitoneally. The radial arm maze and passive avoidance tests were performed to evaluate the animal’s learning and memory. Scopolamine increased the task completing time, the number of total errors (reference and working memory error) in the radial arm maze task, and the latency time in the passive avoidance test, which were significantly ameliorated by treatment with GJD. The GJD treatment also attenuated the scopolamine-induced hyperactivation of acetylcholinesterase activity, and suppression of the expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and their receptors in the hippocampus. These effects of GJD were supported by both the doublecortin (DCX)-positive staining and Nissl staining, which were used to measure hippocampal neurogenesis and atrophy, respectively. These findings strongly suggest that GJD exerts a potent anti-amnesic effect, and its underlying mechanism might involve the modulation of cholinergic activity.
Highlights
As the population ages, the burden of neurodegenerative disorders becomes a globally critical issue
Morroniside and loganin from Cornus cervi parvum were detected at retention time of 3.8 and 5.2 min, respectively
GJD is approved by the Ministry of Food and Drug Safety (MFDS), and annual revenue is estimated to be approximately 46 million USD
Summary
The burden of neurodegenerative disorders becomes a globally critical issue. Among the signs or symptoms of neurodegenerative disorders, memory impairment is the most typical feature, which results from neuronal dysfunction and neuronal loss in the brain tissues, the hippocampal region [2]. The pathogenesis of neurodegenerative disorders still remains uncertain; the deposition of neurofibrillary tangles and/or senile plaques, neuroexcitotoxicity, and cholinergic. Acetylcholine obviously enhances long-term potentiation (LTP) in the basal forebrain and hippocampus [5]. These cholinergic functions are mediated by neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), which maintain neuronal plasticity and synaptogenesis [6]
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