ReferenceID 2206
Loganin prevents chronic constriction injury-provoked neuropathic pain by reducing TNF-α/IL-1β-mediated NF-κB activation and Schwann cell demyelination
Phytomedicine
BACKGROUND: Peripheral nerve injury can produce chronic and ultimately neuropathic pain. The chronic constriction injury (CCI) model has provided a deeper understanding of nociception and chronic pain. Loganin is a well-
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- Reference Id
- 2206
- Evidence Id
- 18796
- Core Evidence Id
- 18796
- Source Reference Id
- 4453
- Herb2 Reference Id
- HBREF005250
- Subject Paper Key
- HBIN033476_31955133
- Pubmed Id
- 31955133
- Doi
- 10.1016/j.phymed.2019.153166
- Paper Title
- Loganin prevents chronic constriction injury-provoked neuropathic pain by reducing TNF-α/IL-1β-mediated NF-κB activation and Schwann cell demyelination
- Paper Abstract
- BACKGROUND: Peripheral nerve injury can produce chronic and ultimately neuropathic pain. The chronic constriction injury (CCI) model has provided a deeper understanding of nociception and chronic pain. Loganin is a well-known herbal medicine with glucose-lowering action and neuroprotective activity. PURPOSE: This study investigated the molecular mechanisms by which loganin reduced CCI-induced neuropathic pain. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham, sham+loganin, CCI and CCI+loganin. Loganin (1 or 5 mg/kg/day) was injected intraperitoneally once daily for 14 days, starting the day after CCI. For behavioral testing, mechanical and thermal responses were assessed before surgery and on d1, d3, d7 and d14 after surgery. Sciatic nerves (SNs) were collected to measure proinflammatory cytokines. Proximal and distal SNs were collected separately for Western blotting and immunofluorescence studies. RESULTS: Thermal hyperalgesia and mechanical allodynia were reduced in the loganin-treated group as compared to the CCI group. Loganin (5 mg/kg/day) prevented CCI from inducing proinflammatory cytokines (TNF-alpha, IL-1beta), inflammatory proteins (TNF-alpha, IL-1beta, pNFkappaB, pIkappaB/IkappaB, iNOS) and receptor (TNFR1, IL-1R), adaptor protein (TRAF2) of TNF-alpha, and Schwann cell demyelination and axonal damage. Loganin also blocked IkappaB phosphorylation (p-IkappaB). Double immunofluorescent staining further demonstrated that pNFkappaB/pIkappaB protein was reduced by loganin in Schwann cells on d7 after CCI. In the distal stumps of injured SN, Schwann cell demyelination was correlated with pain behaviors in CCI rats. CONCLUSION: Our findings indicate that loganin improves CCI-induced neuroinflammation and pain behavior by downregulating TNF-alpha/IL-1beta-dependent NF-kappaB activation.
- Journal
- Phytomedicine
- Publish Year
- 2020
- Experiment Subject
- sprague-dawley rat
- Experiment Type
- Animal Experiment
- Phenotype Related
- Neuropathic Pain; Chronic Constriction Injury; Chronic Pain; Peripheral Nerve Injury; Chronic And Ultimately Neuropathic Pain
- Paper Title Cn
- Paper Title En
- Loganin prevents chronic constriction injury-provoked neuropathic pain by reducing TNF-α/IL-1β-mediated NF-κB activation and Schwann cell demyelination
- Bilingual Status
- semi_complete