Evidence map›Paper›PMID 34512324›Full record

ArticleFrontiers in pharmacology2021

Gallic Acid Alleviates Neuropathic Pain Behaviors in Rats by Inhibiting P2X7 Receptor-Mediated NF-κB/STAT3 Signaling Pathway.

Runan Yang, Zijing Li, Yuting Zou, Jingjian Yang, Lin Li, Xiumei Xu, Günther Schmalzing, Hong Nie, Guilin Li, Shuangmei Liu and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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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 3 institutions in 2 countries.

Runan YangNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Zijing LiUndergraduate Student at the Medical School of Nanchang University, Nanchang, China.
Yuting ZouUndergraduate Student at the Medical School of Nanchang University, Nanchang, China.
Jingjian YangUndergraduate Student at the Medical School of Nanchang University, Nanchang, China.
Lin LiNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Xiumei XuNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Günther SchmalzingInstitute of Clinical Pharmacology, RWTH Aachen University, Aachen, Germany.
Hong NieGuangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, College of Pharmacy, Jinan University, Guangzhou, China.
Guilin LiNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Shuangmei LiuNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Shangdong LiangNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Changshui XuNeuropharmacology Laboratory of Physiology Department, Medical School of Nanchang University, Nanchang, China.
Nanchang University · CNJinan University · CNRWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain is a complex disease with high incidence. Adenosine triphosphate (ATP) and its activated P2X7 receptor are involved in the signal transmission of neuropathic pain. Gallic acid (3,4,5-trihydroxybenzoic acid) is a traditional Chinese medicine obtained from natural plants that exhibit anti-inflammatory, analgesic, and antitumor effects. However, the underlying mechanism for gallic acid in analgesia remains unknown. This study aims to reveal how gallic acid alleviates neuropathic pain behaviors in a rat model with chronic constriction injury (CCI). Real-time PCR, western blotting, double-label immunofluorescence, molecular docking, and whole-cell patch clamp technology were used to explore the therapeutic action of gallic acid on neuropathic pain. The results showed that after CCI rats were treated with gallic acid for 1 week, the mechanical withdrawal threshold and thermal withdrawal latency were increased, accompanied by inhibition of the upregulated expression of P2X7 and TNF-α at both mRNA and protein levels, and reduced NF-κB and phosphorylated-STAT3 in the dorsal root ganglia. At the same time, gallic acid significantly decreased the coexpression of P2X7 and glial fibrillary acidic protein in the dorsal root ganglia. In addition, gallic acid could suppress ATP-activated current in human embryonic kidney 293 (HEK293) cells transfected with the plasmid expressing P2X7 but had no effect on ATP activation current of P2X7-mutant plasmid (with the point mutation sequence of the key site where gallic acid binds to the P2X7 receptor). Therefore, our work suggests that gallic acid may alleviate neuropathic pain in CCI rats by inhibiting the P2X7 receptor and subsequent activation of the TNF-α/STAT3 signaling pathway.

Indexed as

chronic constriction injurydorsal root gangliagallic acidneuropathic painP2X7 receptor

Identifiers

PMID34512324
PMCPMC8423904
OpenAlexW3195616142

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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.