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野山参对东莨菪碱诱导的大鼠海马乙酰胆碱耗竭的影响。

Effect of wild ginseng on scopolamine-induced acetylcholine depletion in the rat hippocampus.

机构信息

Acupuncture and Meridian Science Research Center, Republic of Korea.

出版信息

J Pharm Pharmacol. 2010 Feb;62(2):263-71. doi: 10.1211/jpp.62.02.0015.

DOI:10.1211/jpp.62.02.0015
PMID:20487207
Abstract

OBJECTIVES

The ameliorating effects of wild ginseng on learning and memory deficits were investigated in rats.

METHODS

Rats were treated daily with wild ginseng or cultivated ginseng for 7 days at 30 min before scopolamine injection (2 mg/kg, i.p.). After inducing cognitive impairment by the administration of scopolamine, behavioural assessment using the Morris water maze was performed. Changes in cholinergic system reactivity were also examined by measuring the immunoreactive neurons of choline acetyltransferase and the reactivity of acetylcholinesterase in the hippocampus.

KEY FINDINGS

Scopolamine injection induced impaired performance in the water maze test and severe cell losses in hippocampal cholinergic neurons, as indicated by decreased choline acetyltransferase immunoreactivity and increased acetylcholinesterase reactivity. Daily administration of wild ginseng produced a significant improvement in the escape latency for finding the platform in the Morris water maze and reduced the loss of cholinergic immunoreactivity in the hippocampus. The reduced expression of brain-derived neurotrophic factor mRNA due to the scopolamine injection was recovered to normal levels by the administration of wild ginseng.

CONCLUSIONS

Wild ginseng demonstrates a significant neuroprotective effect against scopolamine-induced neuronal and cognitive impairment.

摘要

目的

研究野山参对大鼠学习记忆缺陷的改善作用。

方法

大鼠在腹腔注射东莨菪碱(2mg/kg)前 30 分钟每天接受野山参或栽培人参治疗 7 天。通过给予东莨菪碱诱导认知障碍后,使用 Morris 水迷宫进行行为评估。通过测量海马胆碱乙酰转移酶的免疫反应性神经元和乙酰胆碱酯酶的反应性,还检查了胆碱能系统反应性的变化。

主要发现

东莨菪碱注射导致水迷宫测试中表现受损,并导致海马胆碱能神经元严重丢失,表现为胆碱乙酰转移酶免疫反应性降低和乙酰胆碱酯酶反应性增加。野山参的每日给药可显著改善 Morris 水迷宫中寻找平台的逃避潜伏期,并减少海马胆碱能免疫反应性的丧失。由于东莨菪碱注射导致脑源性神经营养因子 mRNA 的表达减少,通过野山参给药恢复到正常水平。

结论

野山参对东莨菪碱诱导的神经元和认知障碍具有显著的神经保护作用。

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