ArticleAmerican journal of translational research2026
Spinal manipulative therapy promotes nucleus pulposus resorption and alleviates pain in a rat model of lumbar disc herniation via JNK-dependent regulation of inflammation and tissue remodeling.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Neuroimmune regulation of post-traumatic bone regeneration: focus on inflammatory switching and functional recovery.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLumbar disc herniation (LDH) often resolves spontaneously through inflammation-mediated resorption of the extruded nucleus pulposus (NP). While spinal manipulative therapy (SMT) is clinically used to alleviate LDH-related pain, its role in modulating NP resorption and the underlying molecular mechanisms remain unclear. This study aimed to determine whether SMT promotes NP clearance and to elucidate its signaling pathways.
methodsA rat model of LDH was established by autologous NP implantation onto the L5 nerve root. Animals received either SMT (every other day), epidural betamethasone (SHD, weekly), or sham treatment. Mechanical allodynia was assessed over 28 days. Histology, immunohistochemistry, ELISA, RT-qPCR, and Western blotting were performed on NP tissues. To confirm pathway specificity, experiments were replicated in JNK2-knockout (JNK-KO) mice.
resultsSMT significantly attenuated mechanical allodynia from day 3 onward and promoted near-complete NP resorption by day 28-outperforming SHD in both analgesia and tissue restoration. Unlike SHD's broad anti-inflammatory suppression, SMT maintained a balanced microenvironment: moderately elevating TNF-α, IL-1β, VEGF, and MMP-3 to support macrophage recruitment, neovascularization, and matrix remodeling, while reducing NP cell apoptosis via Bax/Bcl-2 regulation. These effects were accompanied by selective inhibition of NF-κB and MAPK (p38, ERK, JNK) phosphorylation. Crucially, all benefits of SMT were abolished in JNK-KO mice, confirming JNK as an essential upstream mediator.
conclusionSMT promotes pain relief and nucleus pulposus resorption in LDH by inhibiting inflammation and accelerating tissue remodeling through a JNK-dependent mechanism.
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.