Evidence map›Paper›PMID 30254585›Full record

ArticleFrontiers in pharmacology2018

The Effects of Ginsenoside Compound K Against Epilepsy by Enhancing the γ-Aminobutyric Acid Signaling Pathway.

Xiangchang Zeng, Kai Hu, Lulu Chen, Luping Zhou, Wei Luo, Chaopeng Li, Wenjing Zong, Siyu Chen, Qing Gao, Guirong Zeng and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  16. Article
  17. The Effect of Protein-Rich Extract fromMolecules (Basel, Switzerland) · 2020
    Article
  18. Article
  19. Journal of ginseng research · 2019
    Review
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

14 authors at 3 institutions in 1 country.

Xiangchang ZengDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Kai HuDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, China.
Lulu ChenDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Luping ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Wei LuoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Chaopeng LiDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Wenjing ZongDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Siyu ChenDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Qing GaoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Guirong ZengHunan Key Laboratory of Pharmacodynamics and Safety Evaluation of New Drugs & Hunan Provincial Research Center for Safety Evaluation of Drugs, Changsha, China.
Dejian JiangHunan Key Laboratory of Pharmacodynamics and Safety Evaluation of New Drugs & Hunan Provincial Research Center for Safety Evaluation of Drugs, Changsha, China.
Xiaohui LiDepartment of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, China.
Honghao ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Dong-Sheng OuyangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Xiangya Hospital Central South University · CNCentral South University · CNHunan Provincial Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The imbalance between the GABA-mediated inhibition and the glutamate-mediated excitation is the primary pathological mechanism of epilepsy. GABAergic and glutamatergic neurotransmission have become the most important targets for controlling epilepsy. Ginsenoside compound K (GCK) is a main metabolic production of the ginsenoside Rb1, Rb2, and Rc in the intestinal microbiota. Previous studies show that GCK promoted the release of GABA from the hippocampal neurons and enhanced the activity of GABA

Indexed as

epilepsyGABAARα1ginsenoside compound KKCC2neurotransmittersNKCC1

Identifiers

PMID30254585
PMCPMC6142013
OpenAlexW2889437581

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.