ArticleFrontiers in medicine2025
Exploring the mechanism of analgesic effect of Tuina on alleviating delayed muscle soreness in exercise-induced muscle damaged rats: a combined transcriptome- and non-targeted metabolome-based analysis.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Previous research has demonstrated the therapeutic effects of Tuina on exercise-induced muscle damage (EIMD) and its analgesic role in delayed-onset muscle soreness (DOMS). This study aimed to elucidate the molecular mechanisms underlying the analgesic effects of Tuina by analyzing temporal changes in gene expression and metabolite profiles at sites of skeletal muscle injury following intervention. Methods: Eighty-eight 8-week-old SD rats were randomly assigned to a control group (C), an exercise group (E) and a Tuina-treated group (T). An EIMD rat model was established to assess the mechanical withdrawal threshold (MWT), Enzyme-linked immunosorbent assay (ELISA) was employed to measure creatine kinase (CK) levels, histological staining and transmission electron microscopy was used to observed skeletal muscle repair post-Tuina treatment. Transcriptomic and metabolomic analyses were performed to assess dynamic changes in gene expression and metabolites at the sites of muscle micro-damage from 0 to 72 h post-intervention. Results: Tuina significantly increased MWT and reduced CK-MM expression in EIMD rats, indicating enhanced skeletal muscle repair. Transcriptomic analysis identified 470 differentially expressed genes (DEGs) at 48 h post-intervention (E48 vs. T48), enriched in pathways like Chemokine signaling, Leukocyte transendothelial migration, and Regulation of actin cytoskeleton. Metabolomic analysis revealed 761 differentially expressed metabolites (DEMs) at 48 h, enriched in pathways including Inflammatory mediator regulation of TRP channels and cAMP signaling. Integrative analysis pinpointed 35 shared KEGG pathways, highlighting key roles for inflammatory regulation (e.g., Ccl2, Itgam), muscle repair (e.g., Igf1), oxidative stress (Ferroptosis pathway), and cAMP signaling. Conclusion: Tuina alleviates EIMD-associated pain and promotes muscle recovery by modulating inflammatory, promoting tissue repair pathways, inhibiting ferroptosis, and activating cAMP signaling, with the 48 h post-intervention mark representing a critical window for therapeutic effect.
Indexed as
Identifiers
What Socratic 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 Socratic graph.