ArticleNeurochemical research2021
Toll-Like Receptor 2 Antagonist Ameliorates Type 2 Diabetes Mellitus Associated Neuropathic Pain by Repolarizing Pro-inflammatory Macrophages.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Circular RNA circNrip1 Interacts with SYNCRIP to Promote Neuropathic Pain by Stabilizing Tlr2 mRNA in Primary Sensory Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The microbiota-gut-brain axis: novel mechanisms and therapeutic frontiers in obesity and type 2 diabetes.NPJ biofilms and microbiomes · 2026Review
- Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- The pivotal role of immunometabolism in diabetic neuropathy and its potential therapeutic strategies.Frontiers in endocrinology · 2026Review
- Macrophage polarization in diabetic vascular complications: mechanistic insights and therapeutic targets.Journal of translational medicine · 2025Review
- Activation of NR2A-Wnt-TLR2 Signaling Axis in Satellite Glial Cells of the Dorsal Root Ganglion Contributes to Neuropathic Pain Induced by Nerve Injury in Diabetic Mice.Molecular neurobiology · 2025Article
- Fucosylated Glycosaminoglycan Oligosaccharide HS14, Derived from Sea Cucumbers, Is a Novel Inhibitor of Platelet Toll-like Receptor 2.Marine drugs · 2025Article
- The Role of Inflammation in the Pathogenesis of Diabetic Peripheral Neuropathy: New Lessons from Experimental Studies and Clinical Implications.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025Review
- Emerging role of macrophages in neuropathic pain.Journal of orthopaedic translation · 2025Review
- Crumbling Pathogenesis and Biomarkers for Diabetic Peripheral Neuropathy.Biomedicines · 2025Review
- Assessment for Diabetic Neuropathy: Treatment and Neurobiological Perspective.Current diabetes reviews · 2025Review
- Targeting TANK-binding kinase 1 attenuates painful diabetic neuropathy via inhibiting microglia pyroptosis.Cell communication and signaling : CCS · 2024Article
- How inflammation dictates diabetic peripheral neuropathy: An enlightening review.CNS neuroscience & therapeutics · 2024Review
- Involvement of Abnormal p-α-syn Accumulation and TLR2-Mediated Inflammation of Schwann Cells in Enteric Autonomic Nerve Dysfunction of Parkinson's Disease: an Animal Model Study.Molecular neurobiology · 2023Article
- High-fat diet causes mechanical allodynia in the absence of injury or diabetic pathology.Scientific reports · 2022Article
- The crosstalk among TLR2, TLR4 and pathogenic pathways; a treasure trove for treatment of diabetic neuropathy.Inflammopharmacology · 2022Review
- New Advances on Pathophysiology of Diabetes Neuropathy and Pain Management: Potential Role of Melatonin and DPP-4 Inhibitors.Frontiers in pharmacology · 2022Review
- Macrophage as a Peripheral Pain Regulator.Cells · 2021Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Diabetic neuropathy is one of the common complications of type 2 diabetes mellitus (T2DM) with severe outcomes. The mechanisms of physiopathology of diabetic neuropathy are not well elucidated. Inflammation and inflammatory macrophages are recognized to be crucial in diabetic neuropathy. Toll-like receptor 2 (TLR2) is an important factor in innate immune response which could promote the polarization of inflammatory macrophages. In present study, we evaluated the effects of a TLR2 antagonist CU-CPT22 on diabetic neuropathy. We induced T2DM in mice by feeding with high fat diet (HFD). We measured the body weight, blood glucose level, paw withdrawal threshold, inflammatory cytokine production, and macrophages infiltration in T2DM mice. We evaluated the effects of CU-CPT22 on pro-inflammatory cytokines production, macrophage marker expression in lipopolysaccharides (LPS)-treated BMDMs. We administrated CU-CPT22 in T2DM mice and measured the pro-inflammatory cytokines levels, expression of macrophages markers in sciatic nerve (SCN), and paw withdrawal threshold. T2DM mice had significantly increased body weight and blood glucose, and had significantly decreased paw withdrawal threshold. Obvious increased pro-inflammatory cytokine level and infiltration of M1 phenotype macrophages was observed in SCN from T2DM mice. CU-CPT22 prevented pro-inflammatory cytokine production in LPS-treated BMDMs and re-polarized them to M2 phenotype. CU-CPT22 suppressed the inflammation and induced M2 macrophages in SCN from T2DM mice, and ameliorated the paw withdrawal threshold in T2DM mice. CU-CPT22 ameliorates neuropathic pain in T2DM by promoting M2 phenotype macrophages.
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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 OpenQuestion graph.