ArticleThe Korean journal of pain2021
Toll-like receptor 4/nuclear factor-kappa B pathway is involved in radicular pain by encouraging spinal microglia activation and inflammatory response in a rat model of lumbar disc herniation.
Article in The Korean journal of pain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
- Therapeutic and research frontiers in fibromyalgia: integrating pathophysiology with innovative drug repurposing.Inflammopharmacology · 2026Review
- Aggrecan and small leucine-rich proteoglycan fragments correlate with Toll-like receptor-2 mediated inflammation in painful degenerative disc disease.The Korean journal of pain · 2026Article
- Immune system expression profiling in patients experiencing low back pain: A pilot study.PM & R : the journal of injury, function, and rehabilitation · 2026Observational
- Changes in serum pain mediators, stress response, inflammatory markers, and coagulation function in lumbar disc herniation patients treated by musculoskeletal ultrasound-guided needle-knife.Journal of medical biochemistry · 2026Article
- Botulinum Toxin Type A Reduces Pain and NF-κB Levels in a Rat Model of Complex Regional Pain Syndrome.Journal of pain research · 2026Article
- Animal Models of Intervertebral Disc Diseases: Advantages, Limitations, and Future Directions.Neurology international · 2024Review
- TLR-4: a promising target for chemotherapy-induced peripheral neuropathy.Molecular biology reports · 2024Review
- Comparative effect of atorvastatin and risperidone on modulation of TLR4/NF-κB/NOX-2 in a rat model of valproic acid-induced autism.Behavioral and brain functions : BBF · 2024Article
- Exosomes derived from human urine-derived stem cells ameliorate IL-1β-induced intervertebral disk degeneration.BMC musculoskeletal disorders · 2024Article
- Intradiscal inflammatory stimulation induces spinal pain behavior and intervertebral disc degeneration in vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- J147 ameliorates sepsis-induced depressive-like behaviors in mice by attenuating neuroinflammation through regulating the TLR4/NF-κB signaling pathway.Journal of molecular histology · 2023Article
- Hyperbaric Oxygen Therapy Alleviates Paclitaxel-Induced Peripheral Neuropathy Involving Suppressing TLR4-MyD88-NF-κB Signaling Pathway.International journal of molecular sciences · 2023Article
- The role of percutaneous neurolysis in lumbar disc herniation: systematic review and meta-analysis.The Korean journal of pain · 2021Article
- Vitamin D inhibits TNF-α induced apoptosis of human nucleus pulposus cells through regulation of NF-kB signaling pathway.Journal of orthopaedic surgery and research · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLumbar disc herniation (LDH) is a common cause of radicular pain, but the mechanism is not clear. In this study, we investigated the engagement of toll-like receptor 4 (TLR4) and the nuclear factor-kappa B (NF-κB) in radicular pain and its possible mechanisms.
methodsAn LDH model was induced by autologous nucleus pulposus (NP) implantation, which was obtained from coccygeal vertebra, then relocated in the lumbar 4/5 spinal nerve roots of rats. Mechanical and thermal pain behaviors were assessed by using von Frey filaments and hotplate test respectively. The protein level of TLR4 and phosphorylated-p65 (p-p65) was evaluated by western blotting analysis and immunofluorescence staining. Spinal microglia activation was evaluated by immunofluorescence staining of specific relevant markers. The expression of pro- and anti-inflammatory cytokines in the spinal dorsal horn was measured by enzyme linked immunosorbent assay.
resultsSpinal expression of TLR4 and p-NF-κB (p-p65) was significantly increased after NP implantation, lasting up to 14 days. TLR4 was mainly expressed in spinal microglia, but not astrocytes or neurons. TLR4 antagonist TAK242 decreased spinal expression of p-p65. TAK242 or NF-κB inhibitor pyrrolidinedithiocarbamic acid alleviated mechanical and thermal pain behaviors, inhibited spinal microglia activation, moderated spinal inflammatory response manifested by decreasing interleukin (IL)-1β, IL-6, tumor necrosis factor-α expression and increasing IL-10 expression in the spinal dorsal horn.
conclusionsThe study revealed that TLR4/NF-κB pathway participated in radicular pain by encouraging spinal microglia activation and inflammatory response.
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