ArticlePloS one2015
Spinal NF-κB and chemokine ligand 5 expression during spinal glial cell activation in a neuropathic pain model.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Dual CCR2/CCR5 Antagonism with Cenicriviroc Alleviates Nerve Injury-Induced Hypersensitivity and Prevents Morphine Tolerancevia Modulation of Neuroimmune Signaling.Cellular and molecular neurobiology · 2026Article
- Inflammatory and Molecular Mechanisms of Adenomyosis Associated Pain: Insights from Multiple Analytic Approaches.Journal of pain research · 2026Article
- CC Chemokine Family Members' Modulation as a Novel Approach for Treating Central Nervous System and Peripheral Nervous System Injury-A Review of Clinical and Experimental Findings.International journal of molecular sciences · 2024Review
- Targeting Members of the Chemokine Family as a Novel Approach to Treating Neuropathic Pain.Molecules (Basel, Switzerland) · 2023Review
- SAFit2 ameliorates paclitaxel-induced neuropathic pain by reducing spinal gliosis and elevating pro-resolving lipid mediators.Journal of neuroinflammation · 2023Article
- Article
- Spinal Nrf2 translocation may inhibit neuronal NF-κB activation and alleviate allodynia in a rat model of bone cancer pain.Journal of neurochemistry · 2021Article
- Mechanistic Insight into the Effects of Curcumin on Neuroinflammation-Driven Chronic Pain.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Therapeutic effects of peripherally administrated neural crest stem cells on pain and spinal cord changes after sciatic nerve transection.Stem cell research & therapy · 2021Article
- Blockade of CC Chemokine Receptor Type 3 Diminishes Pain and Enhances Opioid Analgesic Potency in a Model of Neuropathic Pain.Frontiers in immunology · 2021Article
- NF-κB p65-dependent transcriptional regulation of histone deacetylase 2 contributes to the chronic constriction injury-induced neuropathic pain via the microRNA-183/TXNIP/NLRP3 axis.Journal of neuroinflammation · 2020Article
- RETRACTED: Ultramicronized Palmitoylethanolamide and Paracetamol, a New Association to Relieve Hyperalgesia and Pain in a Sciatic Nerve Injury Model in Rat.International journal of molecular sciences · 2020Article
- IL-1β Induced Cytokine Expression by Spinal Astrocytes Can Play a Role in the Maintenance of Chronic Inflammatory Pain.Frontiers in physiology · 2020Article
- Effect of PKC/NF-Pain research & management · 2020Article
- Article
- The Chemokine CCL4 (MIP-1β) Evokes Antinociceptive Effects in Mice: a Role for CD4Molecular neurobiology · 2019Article
- Effect of PEA-OXA on neuropathic pain and functional recovery after sciatic nerve crush.Journal of neuroinflammation · 2018Article
- Activation of dorsal horn cannabinoid CB2 receptor suppresses the expression of P2YJournal of neuroinflammation · 2017Article
- Immune dysregulation in patients with carpal tunnel syndrome.Scientific reports · 2017Article
- Inhibition of spinal UCHL1 attenuates pain facilitation in a cancer-induced bone pain model by inhibiting ubiquitin and glial activation.American journal of translational research · 2016Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe NF-κB pathway and chemokine (C-C motif) ligand 5 (CCL5) are involved in pain modulation; however, the precise mechanisms of their interactions in chronic neuropathic pain have yet to be established.
methodsThe present study examined the roles of spinal NF-κB and CCL5 in a neuropathic pain model after chronic constriction injury (CCI) surgery. CCI-induced pain facilitation was evaluated using the Plantar and von Frey tests. The changes in NF-κB and CCL5 expression were analyzed by immunohistochemistry and Western blot analyses.
resultsSpinal NF-κB and CCL5 expression increased after CCI surgery. Repeated intrathecal infusions of pyrrolidine dithiocarbamate (PDTC, a NF-κB inhibitor) decreased CCL5 expression, inhibited the activation of microglia and astrocytes, and attenuated CCI-induced allodynia and hyperalgesia. Intrathecal injection of a CCL5-neutralizing antibody attenuated CCI-induced pain facilitation and also suppressed spinal glial cell activation after CCI surgery. However, the CCL5-neutralizing antibody did not affect NF-κB expression. Furthermore, selective glial inhibitors, minocycline and fluorocitrate, attenuated the hyperalgesia induced by intrathecal CCL5.
conclusionsThe inhibition of spinal CCL5 expression may provide a new method to prevent and treat nerve injury-induced neuropathic pain.
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