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The ethanolic extract of Aralia continentalis ameliorates cognitive deficits via modifications of BDNF expression and anti-inflammatory effects in a rat model of post-traumatic stress disorder

Authors
Lee, BombiHong, RiwonLim, PooreumCho, DaeunYeom, MijungLee, SanghyunKang, Ki SungLee, Sang CheonShim, InsopLee, HyejungHahm, Dae-Hyun
Issue Date
8-Jan-2019
Publisher
BMC
Keywords
Aralia continentalis; Post-traumatic stress disorder; Memory; Brain-derived neurotrophic factor; Pro-inflammatory cytokines
Citation
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE, v.19
Journal Title
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
Volume
19
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/1951
DOI
10.1186/s12906-018-2417-0
ISSN
1472-6882
Abstract
BackgroundPost-traumatic stress disorder (PTSD) is a disease associated with that the experience of traumatic stress. The traumatic experience results in the development of a prolonged stress response that causes impaired memory function and increased inflammation in the hippocampus. Currently, antidepressants are the only approved therapy for PTSD. However, the efficacy of antidepressants in the treatment of PTSD is marginal. The ethanol extract of Aralia continentalis (AC) is traditionally used in oriental medicine, and has been showed to possess pharmacological properties, including anti-inflammatory, anti-cancer, anti-atherosclerotic, and anti-diabetic effects. Nevertheless, the effects of AC on cognitive memory and its mechanism of action in PTSD remain unclear. Given the necessity of further treatment options for PTSD, we investigated the effect of AC on the spatial cognitive impairment caused by single prolonged stress (SPS) in a rat model of PTSD.MethodsMale rats were treated with various intraperitoneal (i.p.) doses of AC for 21 consecutive days after inducing chronic stress with the SPS procedure.ResultsCognitive impairment caused by SPS were inhibited after treatment with 100mg/kgAC, as measured by the Morris water maze test and an object recognition test. Additionally, AC treatment significantly alleviated memory-related decreases in brain-derived neurotrophic factor (BDNF) mRNA and protein levels in the hippocampus. Our results suggest that AC significantly inhibited the cognitive deficits caused by SPS via increased expression of pro-inflammatory cytokines, including tumor necrosis factor- and interleukin-6, in the rat brain.ConclusionsAC reversed the behavioral impairments and inflammation triggered by SPS-derived traumatic stress and should be further evaluated as a potential therapeutic drug for PTSD.
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College of Korean Medicine (Premedical course of Oriental Medicine)
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