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杠柳的乙醇提取物通过改变 BDNF 表达和发挥抗炎作用改善创伤后应激障碍大鼠模型的认知障碍。

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.

机构信息

Acupuncture and Meridian Science Research Center, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.

The Graduate School of Basic Science of Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.

出版信息

BMC Complement Altern Med. 2019 Jan 8;19(1):11. doi: 10.1186/s12906-018-2417-0.

Abstract

BACKGROUND

Post-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.

METHODS

Male rats were treated with various intraperitoneal (i.p.) doses of AC for 21 consecutive days after inducing chronic stress with the SPS procedure.

RESULTS

Cognitive impairment caused by SPS were inhibited after treatment with 100 mg/kg AC, 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-α and interleukin-6, in the rat brain.

CONCLUSIONS

AC reversed the behavioral impairments and inflammation triggered by SPS-derived traumatic stress and should be further evaluated as a potential therapeutic drug for PTSD.

摘要

背景

创伤后应激障碍(PTSD)是一种与创伤性应激经历相关的疾病。创伤性经历导致长期应激反应的发展,从而导致海马体记忆功能受损和炎症增加。目前,抗抑郁药是治疗 PTSD 的唯一批准疗法。然而,抗抑郁药在治疗 PTSD 方面的疗效有限。辽东楤木(AC)的乙醇提取物在东方医学中被传统使用,并且已经显示出具有药理学特性,包括抗炎、抗癌、抗动脉粥样硬化和抗糖尿病作用。然而,AC 对认知记忆的影响及其在 PTSD 中的作用机制尚不清楚。鉴于 PTSD 进一步治疗选择的必要性,我们研究了 AC 对 PTSD 大鼠模型中单延长应激(SPS)引起的空间认知障碍的影响。

方法

雄性大鼠在 SPS 程序诱导慢性应激后连续 21 天每天接受不同剂量的腹腔(i.p.)AC 治疗。

结果

SPS 引起的认知障碍在用 100mg/kg AC 治疗后得到抑制,通过 Morris 水迷宫测试和物体识别测试测量。此外,AC 治疗显著减轻了 SPS 引起的海马体脑源性神经营养因子(BDNF)mRNA 和蛋白水平相关的记忆下降。我们的研究结果表明,AC 通过增加大鼠脑中促炎细胞因子(包括肿瘤坏死因子-α和白细胞介素-6)的表达,显著抑制了 SPS 引起的认知缺陷。

结论

AC 逆转了 SPS 引起的创伤性应激触发的行为损伤和炎症,应进一步评估其作为 PTSD 潜在治疗药物的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5446/6323859/cbe2f7015e93/12906_2018_2417_Fig1_HTML.jpg

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