Inhaled essential oil fromChamaecyparis obtuseameliorates the impairments of cognitive function induced by injection of β-amyloid in rats

神经毒性 莫里斯水上航行任务 药理学 乙酰胆碱酯酶 海马体 中枢神经系统 标记法 细胞凋亡 化学 抗氧化剂 阿切 医学 毒性 内分泌学 生物化学 内科学
作者
Donghyuck Bae,Heejin Seol,Ho‐Geun Yoon,Ju-Ryun Na,Kyonyeo Oh,Chul Yung Choi,Dong-Wook Lee,Woojin Jun,Kwang Youl Lee,Jeongmin Lee,Kwontack Hwang,Yoo‐Hyun Lee,Sunoh Kim
出处
期刊:Pharmaceutical Biology [Taylor & Francis]
卷期号:50 (7): 900-910 被引量:34
标识
DOI:10.3109/13880209.2011.642886
摘要

Context: Chamaecyparis obtusa Sieb. & Zucc., Endlicher (Cupressaceae) forest bathing or aromatherapy has been shown in various studies to have biological functions such as anticancer, antiallergies, antiinflammatory, and antioxidant activity. However, no reports exist on the pharmacological or biological activities of the essential oil of C. obtusa (EOCO) or its effects on central nervous system.Objective: The aggregation and formation of β-amyloid peptides (Aβ) into fibrils are central events in the pathogenesis of Alzheimer's disease (AD), and overproduction and aggregation of Aβ into oligomers have been known to trigger neurotoxicity. In this study, we investigated the effects of inhaled EOCO on cognitive function and neuronal apoptosis in rats intrahippocampally injected with Aβ.Materials and methods: To model AD, 4 μg of aggregated Aβ was injected into the hippocampus. To test the effects of EOCO, behavioral performance in the Morris water maze was tested 4 days after injection. After behavioral testing, brain sections were prepared for TTC staining and TUNEL assay.Results: Inhaled EOCO protected spatial learning and memory from the impairments induced by Aβ1–40 injection. In addition, the behavioral deficits accompanying Aβ1–40-induced AD were attenuated by inhalation of EOCO. Furthermore, acetylcholinesterase (AChE) activity and neuronal apoptosis were significantly inhibited in rats treated with Aβ1–40 and EOCO compared to rats treated only with Aβ1–40.Discussion and conclusion: EOCO suppressed both AD-related neuronal cell apoptosis and AD-related dysfunction of the memory system. Thus, the results of this study support EOCO as a candidate drug for the treatment of AD.
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