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人参总皂苷通过干预 GSK-3β-CREB 信号通路逆转皮质酮诱导的抑郁样行为及海马可塑性相关蛋白的改变。

Ginseng Total Saponins Reverse Corticosterone-Induced Changes in Depression-Like Behavior and Hippocampal Plasticity-Related Proteins by Interfering with GSK-3 β -CREB Signaling Pathway.

机构信息

Basic Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, China.

Basic Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, China ; Laboratory of Pathological Sciences, Basic Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, China.

出版信息

Evid Based Complement Alternat Med. 2014;2014:506735. doi: 10.1155/2014/506735. Epub 2014 Jan 9.

DOI:10.1155/2014/506735
PMID:24523822
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3913067/
Abstract

This study aimed to explore the antidepressant mechanisms of ginseng total saponins (GTS) in the corticosterone-induced mouse depression model. In Experiment 1, GTS (50, 25, and 12.5 mg kg(-1) d(-1), intragastrically) were given for 3 weeks. In Experiment 2, the same doses of GTS were administrated after each corticosterone (20 mg kg(-1) d(-1), subcutaneously) injection for 22 days. In both experiments, mice underwent a forced swimming test and a tail suspension test on day 20 and day 21, respectively, and were sacrificed on day 22. Results of Experiment 1 revealed that GTS (50 and 25 mg kg(-1) d(-1)) exhibited antidepressant activity and not statistically altered hippocampal protein levels of brain-derived neurotrophic factor (BDNF) and neurofilament light chain (NF-L). Results of Experiment 2 showed that GTS (50 and 25 mg kg(-1) d(-1)) ameliorated depression-like behavior without normalizing hypercortisolism. The GTS treatments reversed the corticosterone-induced changes in mRNA levels of BDNF and NF-L, and protein levels of BDNF NF-L, phosphor-cAMP response element-binding protein (Ser133), and phosphor-glycogen synthase kinase-3 β (Ser9) in the hippocampus. These findings imply that the effect of GTS on corticosterone-induced depression-like behavior may be mediated partly through interfering with hippocampal GSK-3 β -CREB signaling pathway and reversing decrease of some plasticity-related proteins.

摘要

本研究旨在探讨人参总皂苷(GTS)在皮质酮诱导的小鼠抑郁模型中的抗抑郁作用机制。实验 1 中,GTS(50、25 和 12.5mg·kg(-1)·d(-1),灌胃)连续给药 3 周。实验 2 中,在连续 22 天每天给予 20mg·kg(-1)·d(-1)的皮质酮(皮下注射)后,给予相同剂量的 GTS。在两个实验中,小鼠分别于第 20 天和第 21 天进行强迫游泳试验和悬尾试验,第 22 天处死。实验 1 的结果表明,GTS(50 和 25mg·kg(-1)·d(-1))表现出抗抑郁活性,而海马脑源性神经营养因子(BDNF)和神经丝轻链(NF-L)的蛋白水平没有统计学改变。实验 2 的结果显示,GTS(50 和 25mg·kg(-1)·d(-1))改善了抑郁样行为,而没有使皮质醇过度升高正常化。GTS 处理逆转了皮质酮诱导的 BDNF 和 NF-L mRNA 水平以及 BDNF、NF-L、磷酸化 cAMP 反应元件结合蛋白(Ser133)和磷酸化糖原合酶激酶-3β(Ser9)蛋白水平的变化。这些发现表明,GTS 对皮质酮诱导的抑郁样行为的影响可能部分通过干扰海马 GSK-3β-CREB 信号通路和逆转一些与可塑性相关蛋白的减少来介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/a142e2677631/ECAM2014-506735.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/b0a3018bd9a8/ECAM2014-506735.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/f46a4ccd85c0/ECAM2014-506735.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/14d4a9d8f2c6/ECAM2014-506735.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/70b6fbe31695/ECAM2014-506735.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/269d4ff2f88f/ECAM2014-506735.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/a142e2677631/ECAM2014-506735.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/b0a3018bd9a8/ECAM2014-506735.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/f46a4ccd85c0/ECAM2014-506735.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/14d4a9d8f2c6/ECAM2014-506735.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/70b6fbe31695/ECAM2014-506735.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/269d4ff2f88f/ECAM2014-506735.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfce/3913067/a142e2677631/ECAM2014-506735.006.jpg

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