ArticleJournal of cellular and molecular medicine2026
Tuina Inhibits Synaptic Plasticity Through the Astrocytic NDRG2/GLT-1 Pathway to Alleviate Neuropathic Pain.
Article in Journal of cellular and molecular medicine, 2026. 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
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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.
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Who cites it
2 citing papers in PubMed.
- Astrocytes in Neuropathic Pain: Mechanistic and Global Insights.Pain research & management · 2026Review
- Tuina Inhibits Synaptic Plasticity Through the Astrocytic NDRG2/GLT-1 Pathway to Alleviate Neuropathic Pain.Journal of cellular and molecular medicine · 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
8 authors.
Funding
Abstract
While Tuina has demonstrated clinical efficacy in alleviating neuropathic pain (NP) induced by peripheral nerve injury, the underlying molecular mechanisms remain unclear. Synaptic plasticity in the spinal dorsal horn (SDH) is a key regulator of pain processing, wherein astrocytes play a central role. Regulation of N-myc downstream-regulated gene 2 (NDRG2) and glutamate transporter 1 (GLT-1) is particularly important in NP modulation. Accumulating evidence suggests that Tuina exerts analgesic effects by inhibiting aberrant synaptic plasticity. This study explored whether Tuina regulates synaptic plasticity through astrocytes to attenuate NP. Using an in vivo model, Tuina or the astrocytic inhibitor fluorocitrate was administered to a chronic constriction injury (CCI)-induced NP rat model for 14 days. Tuina significantly alleviated pain hypersensitivity in CCI rats, improved structural damage, suppressed astrocytic activation, reduced glutamate accumulation and restored the SDH's expression of proteins linked to synaptic plasticity. These effects were associated with inhibition of astrocytic NDRG2 and upregulation of GLT-1. Conversely, NDRG2 overexpression through AAV impaired Tuina's ability to promote glutamate transport, leading to glutamate accumulation, enhanced excitatory transmission and reduced analgesic efficacy. In conclusion, Tuina alleviates NP by modulating the astrocytic NDRG2/GLT-1 pathway, reducing synaptic glutamate levels and normalising synaptic plasticity. These findings provide new mechanistic insights into Tuina's analgesic action and have identified NDRG2/GLT-1 as a possible therapeutic target for NP treatment.
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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.