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人参根中的倍半萜类化合物通过脑源性神经营养因子/原肌球蛋白相关激酶B和沉默调节蛋白1/核因子-κB信号通路减轻脂多糖诱导的抑郁样行为。

Sesquiterpenoids from the Root of Panax ginseng Attenuates Lipopolysaccharide-Induced Depressive-Like Behavior through the Brain-Derived Neurotrophic Factor/Tropomyosin-Related Kinase B and Sirtuin Type 1/Nuclear Factor-κB Signaling Pathways.

作者信息

Wang Weidong, Liu Xiaofeng, Liu Jinping, Cai Enbo, Zhao Yan, Li Haijun, Zhang Lianxue, Li Pingya, Gao Yugang

机构信息

College of Chinese Medicinal Materials, Jilin Agricultural University , Changchun, Jilin 130118, People's Republic of China.

Ningxia People's Hospital , Yinchuan, Ningxia 750021, People's Republic of China.

出版信息

J Agric Food Chem. 2018 Jan 10;66(1):265-271. doi: 10.1021/acs.jafc.7b04835. Epub 2017 Dec 21.

DOI:10.1021/acs.jafc.7b04835
PMID:29237268
Abstract

The previous study indicated sesquiterpenoids from the root of Panax ginseng (SPG) exhibited a significant antidepressant-like effect, which might be mediated by the modification of the dopaminergic, GABAergic, and glutamatergic systems. This study was to investigate antidepressant effects and mechanisms on the lipopolysaccharide (LPS)-induced depression-like behavior of SPG. In the tail suspension test (TST) and forced swimming test (FST), SPG (0.25 and 1 mg/kg, i.g.) and fluoxetine (20 mg/kg, i.p.) effectively reduced the immobility time. SPG treatment significantly reduced serum levels of IL-6 and TNF-α and increased suppressed superoxide dismutase (SOD) activity in the hippocampus. In addition, SPG effectively upregulated the brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB), and sirtuin type 1 (Sirt 1) expression in the hippocampus and downregulated the inhibitor of κB-α (IκB-α) and nuclear factor-κB (NF-κB) phosphorylation. These results suggested that SPG exhibited an antidepressant-like effect through the BDNF/TrkB and Sirt 1/NF-κB signaling pathways.

摘要

先前的研究表明,人参根中的倍半萜类化合物(SPG)具有显著的抗抑郁样作用,这可能是通过调节多巴胺能、γ-氨基丁酸能和谷氨酸能系统介导的。本研究旨在探讨SPG对脂多糖(LPS)诱导的抑郁样行为的抗抑郁作用及其机制。在悬尾试验(TST)和强迫游泳试验(FST)中,SPG(0.25和1mg/kg,灌胃)和氟西汀(20mg/kg,腹腔注射)有效缩短了不动时间。SPG治疗显著降低了血清白细胞介素-6和肿瘤坏死因子-α水平,并增加了海马中被抑制的超氧化物歧化酶(SOD)活性。此外,SPG有效上调了海马中脑源性神经营养因子(BDNF)、原肌球蛋白相关激酶B(TrkB)和沉默调节蛋白1(Sirt 1)的表达,并下调了κB-α抑制因子(IκB-α)和核因子-κB(NF-κB)的磷酸化。这些结果表明,SPG通过BDNF/TrkB和Sirt 1/NF-κB信号通路发挥抗抑郁样作用。

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