Evidence map›Paper›PMID 37631068›Full record

ArticlePharmaceuticals (Basel, Switzerland)2023

Gypenoside-14 Reduces Depression via Downregulation of the Nuclear Factor Kappa B (NF-kB) Signaling Pathway on the Lipopolysaccharide (LPS)-Induced Depression Model.

Yaqun Jiang, Xiang Cheng, Ming Zhao, Tong Zhao, Mengya Zhang, Zibi Shi, Xiangpei Yue, Yanan Geng, Jiayue Gao, Chengbo Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  8. Mechanisms of gypenosides in type 2 diabetes mellitus via regulation of m6A methylase METTL3/14 and demethylase FTO.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 1 country.

Yaqun JiangSchool of Pharmaceutical Sciences, University of South China, Hengyang 421001, China.
Xiang ChengBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Ming ZhaoBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Tong ZhaoBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Mengya ZhangSchool of Pharmaceutical Sciences, University of South China, Hengyang 421001, China.
Zibi ShiBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Xiangpei YueBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Yanan GengBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Jiayue GaoBeijing Institute of Basic Medical Sciences, Beijing 100850, China.
Chengbo WangCAS Key Laboratory of Chemistry of Northwestern Plant Resources and Key Laboratory for Natural Medicine of Gansu Province, Lanzhou Institute of Chemical Physics (LICP), Chinese Academy of Sciences (CAS), Lanzhou 730000, China.
Junli YangCAS Key Laboratory of Chemistry of Northwestern Plant Resources and Key Laboratory for Natural Medicine of Gansu Province, Lanzhou Institute of Chemical Physics (LICP), Chinese Academy of Sciences (CAS), Lanzhou 730000, China.
Lingling ZhuSchool of Pharmaceutical Sciences, University of South China, Hengyang 421001, China.
Institute of Basic Medical Sciences of the Chinese Academy of Medical SciencesBeijing Institute of Education · CNChinese Academy of Sciences · CNUniversity of South China · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is a common pathogenetic sign of depression and is closely linked to the development of depression. Many clinical anti-inflammatory drugs act as antidepressants by reducing the neuroinflammatory response. Previous research found that gypenosides and their bioactive compound gypenoside-14 (GP-14) had neuroprotective effects against hypoxia-induced injury and reduced neuroinflammation-related high-altitude cerebral edema. Here we investigated the effects of GP-14 on the lipopolysaccharide (LPS)-induced depression-like behavior model. LPS (0.5 mg/kg) was injected into mice intraperitoneally for 7 consecutive days to induce depression-like behavior, which is considered a model for the exacerbation of depression. GP-14 in the amount of 100 mg/kg was simultaneously administered by gavage for 7 days. In the LPS-induced depression model, GP-14 not only attenuated depression-like behavior but also improved the anxiety-like behavior of the mice. Additionally, GP-14 treatment mitigated learning and cognitive decline in depressed mice. ELISA and immunofluorescence staining results revealed that GP-14 inhibited the upregulation of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), and suppressed the activation of astrocytes induced with LPS, indicating its potent anti-inflammatory effect. GP-14 pretreatment in C8 cells and primary astrocytes can inhibit the activation of the NF-κB signaling pathway and downregulate the levels of pro-inflammatory factors. In summary, our findings showed that GP-14 had significant anti-inflammation and anti-depression properties; thus, GP-14 could be a promising lead compound for treating depression.

Indexed as

astrocytedepressiongypenoside-14 (GP-14)lipopolysaccharideneuroinflammation

Identifiers

PMID37631068
PMCPMC10459727
OpenAlexW4385811889

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.