ArticleMolecular pain
Electroacupuncture reduces visceral pain and anxiety associated with inflammatory bowel disease by inhibition of vHPC-to-mPFC pathway.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Bioactive compounds for neuroinflammation and neuropathic pain management: molecular and cellular mechanisms.Inflammopharmacology · 2026Review
- Exosomal Adiponectin Plays a Role in Electroacupuncture Analgesia by Activating the Adiponectin Receptor 1 to Inhibit Pain-Related Pathways in Mice Brain.Pain research & management · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EA effectively treats gastrointestinal diseases, pain symptoms, and emotional disorder. Furthermore, vHPC and mPFC are two of the crucial nuclei involved in controlling chronic pain and anxiety-like behaviors. In the present study, it is investigated whether EA may reduce visceral pain and anxiety associated with inflammatory bowel disease (IBD) by inhibition of vHPC-to-mPFC pathway. We found that EA alleviated visceral hyperalgesia and anxiety in TNBS-treated IBD mice. EA decreased the numbers of c-Fos and neurogranin (labeled glutamatergic neurons) co-labeled neurons in both vHPC and mPFC. EA suppressed the activation of vHPC and mPFC pyramidal neurons associated with anxiety-like behaviors and EA suppressed the activation of vHPC neuronal response to von Frey filament. In addition, chemogenetic inhibition of the vHPC-to-mPFC pathway alleviated mechanical allodynia, visceral hyperalgesia and anxiety in IBD mice. However, chemogenetic activation of vHPC-to-mPFC pathway antagonized the effect of EA on anxiety and visceral hyperalgesia, but not on mechanical allodynia in IBD mice. In conclusion, our findings revealed that vHPC-to-mPFC pathway is involved in the inhibitory effect of EA on anxiety and pain sensitivity in IBD mice. EA may exert anti-anxiety effect via inhibition of vHPC-to-mPFC pathway. Thus, our study provides new information about the cellular circuits mechanisms of the therapeutic effect of EA on the comorbidity of visceral pain and anxiety induced by IBD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.