ArticleFrontiers in molecular neuroscience2026
Tuina therapy alleviates neuropathic pain by modulating the CX3CL1/CX3CR1 axis to inhibit degradation of the perineuronal nets.
Article in Frontiers in molecular neuroscience, 2026. 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
Introduction: Tuina, a traditional Chinese non-pharmacological therapy, is effective in treating neuropathic pain (NP). However, its underlying molecular mechanisms remain elusive. The degradation of perineuronal nets (PNNs) via the CX3CL1/CX3CR1 axis is a key driver of central sensitization. This study investigates whether Tuina exerts analgesia by modulating this specific neuro-immune axis to preserve PNNs integrity in a rat model of chronic compression of the dorsal root ganglion (CCD). Methods: Sprague-Dawley rats were subjected to CCD surgery to establish the NP model. To validate the role of PNNs, a subset of rats received intrathecal chondroitinase ABC (chABC). To explore Tuina's mechanism, rats were divided into Sham, Model, Tuina, CX3CR1 inhibitor (AZD8797), and Tuina + AZD8797 groups. Standardized Tuina intervention or inhibitor administration was performed from days 4 to 14 post-surgery. Pain behaviors (PWT and PWL) were evaluated. Spinal dorsal horn tissues were analyzed using transmission electron microscopy, Western blotting, immunofluorescence, and flow cytometry. Results: CCD induced severe mechanical allodynia and thermal hyperalgesia, accompanied by the structural disruption of spinal PNNs-indicated by a significant loss of WFA-binding glycosaminoglycans despite unchanged total aggrecan core protein levels-and ultrastructural neuronal damage. Mechanistically, CCD upregulated the CX3CL1/CX3CR1/PI3K/AKT cascade, which was associated with increased markers of microglial phagocytosis (upregulated TREM2 and LAMP1), as well as Ca Conclusion: Tuina produces robust central analgesia by suppressing the CX3CL1/CX3CR1-PI3K/AKT signaling pathway. This suppression restores microglial phagocytic homeostasis and crucially protects the glycosaminoglycan lattice of PNNs against excessive degradation, thereby alleviating neuropathic central sensitization.
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.