Evidence map›Paper›PMID 35087409›Full record

ArticleFrontiers in pharmacology2021

Aprepitant Inhibits JNK and p38/MAPK to Attenuate Inflammation and Suppresses Inflammatory Pain.

Yang Yang, Wei Zhou, Xiuqi Xu, Xianxiu Ge, Fei Wang, Guang-Qin Zhang, Lin Miao, Xueting Deng

Open access · goldAbstract read
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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  9. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
    Review
  10. Article
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  12. Review
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  14. Article
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  18. Aprepitant Restores Corneal Sensitivity and Reduces Pain in DED.Translational vision science & technology · 2024
    Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Yang YangMedical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Wei ZhouDepartment of Child Health Care, Children's Hospital of Nanjing Medical University, Nanjing, China.
Xiuqi XuDepartment of Clinical Pharmacy, China Pharmaceutical University, Nanjing, China.
Xianxiu GeMedical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Fei WangMedical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Guang-Qin ZhangDepartment of Clinical Pharmacy, China Pharmaceutical University, Nanjing, China.
Lin MiaoMedical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Xueting DengMedical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Second Affiliated Hospital of Nanjing Medical University · CNChina Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Substance P contributes to the pathogenesis of pain by acting on NK-1R, specialized sensory neurons that detect noxious stimuli. Aprepitant, an antagonist of NK-1R, is widely used to treat chemotherapy-induced nausea and vomiting. In this study, we used LPS-stimulated BV-2 microglia cell line and animal models of inflammatory pain to explore the analgesic effect of aprepitant on inflammatory pain and its underlying mechanism. The excitability of DRG neurons were measured using whole-cell patch-clamp recordings. The behavioral tests were measured and the morphological changes on inflamed paw sections were determined by HE staining. Changes in the expressions of cytokine were measured by using real-time quantitative PCR analysis and ELISA method. Immunofluorescence and western blotting were used to detect the microglia activation and MAPK. Aprepitant treatment significantly inhibited the excitability of DRG neurons. The pain behavior and the paw tissues inflammatory damage were significantly relived after the administration of aprepitant compared to formalin group. Aprepitant significantly suppressed the activation of microglia, phosphorylation of JNK and p38 MAPK, as well as the mRNA and protein expressions of MCP-1, TNF-α, IL-6, and IL-1β,

Indexed as

aprepitantinflammatory painJNKNFκBp38

Identifiers

PMID35087409
PMCPMC8786910
OpenAlexW4205798838

What Socratic 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 Socratic graph.