Evidence map›Paper›PMID 27296622›Full record

ArticleMolecular pain2016

Go-sha-jinki-Gan (GJG) ameliorates allodynia in chronic constriction injury-model mice via suppression of TNF-α expression in the spinal cord.

Miho Nakanishi, Aya Nakae, Yuki Kishida, Kousuke Baba, Noriko Sakashita, Masahiko Shibata, Hideki Yoshikawa, Keisuke Hagihara

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

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  15. P2YJournal of pain research · 2017
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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

8 authors at 1 institution in 1 country.

Miho NakanishiOsaka University Graduate School of medicine.
Aya NakaeOsaka University Graduate School of medicineOsaka University Graduate School of medicineOsaka University Graduate School of medicineOsaka University Graduate School of medicine Osaka University Graduate School of Medicine Osaka University Graduate School of Medicine.
Yuki KishidaOsaka University Graduate School of medicine.
Kousuke BabaOsaka University Graduate School of medicine.
Noriko SakashitaOsaka University Graduate School of medicine.
Masahiko ShibataOsaka University Graduate School of Medicine.
Hideki YoshikawaOsaka University Graduate School of Medicine.
Keisuke HagiharaOsaka University Graduate School of medicineOsaka University Graduate School of medicineOsaka University Graduate School of medicineOsaka University Graduate School of medicine Osaka University Graduate School of Medicine Osaka University Graduate School of Medicine hagihara.keisuke@gmail.com.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlternative medicine is noted for its clinical effect and minimal invasiveness in the treatment of neuropathic pain. Go-sha-jinki-Gan, a traditional Japanese herbal medicine, has been used for meralgia and numbness in elderly patients. However, the exact mechanism of GJG is unclear. This study aimed to investigate the molecular mechanism of the analgesic effect of GJG in a chronic constriction injury model.

resultsGJG significantly reduced allodynia and hyperalgesia from the early phase (von Frey test, p<0.0001; cold-plate test, p<0.0001; hot-plate test p¼0.011; two-way repeated measures ANOVA). Immunohistochemistry and Western blot analysis revealed that GJG decreased the expression of Iba1 and tumor necrosis factor-a in the spinal cord. Double staining immunohistochemistry showed that most of the tumor necrosis factor-a was co-expressed in Iba1-positive cells at day 3 post-operation. GJG decreased the phosphorylation of p38 in the ipsilateral dorsal horn. Moreover, intrathecal injection of tumor necrosis factor-a opposed the anti-allodynic effect of GJG in the cold-plate test.

conclusionsOur data suggest that GJG ameliorates allodynia in chronic constriction injury model mice via suppression of tumor necrosis factor-a expression derived from activated microglia. GJG is a promising drug for the treatment of neuropathic pain induced by neuro-inflammation.

Indexed as

AnimalsBehavior, AnimalChromatography, High Pressure LiquidCold TemperatureConstrictionDisease Models, AnimalDrugs, Chinese HerbalHyperalgesiaInjections, SpinalMaleMice, Inbred C57BLMicrogliaSpinal CordTumor Necrosis Factor-alphaDrugs, Chinese Herbalgosha-jinki-ganTumor Necrosis Factor-alpha

Identifiers

PMID27296622
PMCPMC4956397
OpenAlexW2433708706

What OpenQuestion holds

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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.