ArticleBritish journal of pharmacology2011
Anti-nociceptive effect of kinin B₁ and B₂ receptor antagonists on peripheral neuropathy induced by paclitaxel in mice.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Ion Channels and G-Protein-Coupled Receptors Involved in the Development of Chronic Post-ischemic Pain (CPIP): A Model of Complex Regional Pain Syndrome (CRPS-I).Molecular neurobiology · 2025Review
- Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms.Circulation research · 2025Article
- HDAC inhibitors as a potential therapy for chemotherapy-induced neuropathic pain.Inflammopharmacology · 2024Review
- Centralizing the Knowledge and Interpretation of Pain in Chemotherapy-Induced Peripheral Neuropathy: A Paradigm Shift towards Brain-Centric Approaches.Brain sciences · 2024Review
- Kinin BPharmaceuticals (Basel, Switzerland) · 2023Article
- Review
- Kinin BPharmaceutics · 2023Article
- Kinin BScientific reports · 2023Article
- Kinin BPharmaceutics · 2023Article
- Systemic, Intrathecal, and Intracerebroventricular Antihyperalgesic Effects of the Calcium Channel Blocker CTK 01512-2 Toxin in Persistent Pain Models.Molecular neurobiology · 2022Article
- Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy.Frontiers in molecular biosciences · 2021Review
- Bradykinin Receptors Play a Critical Role in the Chronic Post-ischaemia Pain Model.Cellular and molecular neurobiology · 2021Article
- Taxane-induced neurotoxicity: Pathophysiology and therapeutic perspectives.British journal of pharmacology · 2020Review
- Reciprocal Regulatory Interaction between TRPV1 and Kinin B1 Receptor in a Rat Neuropathic Pain Model.International journal of molecular sciences · 2020Article
- Pharmacological Treatment of Chemotherapy-Induced Neuropathic Pain: PPARγ Agonists as a Promising Tool.Frontiers in neuroscience · 2019Review
- Circulating microRNA and automated motion analysis as novel methods of assessing chemotherapy-induced peripheral neuropathy in mice.PloS one · 2019Article
- Genome-wide association study identifies genes associated with neuropathy in patients with head and neck cancer.Scientific reports · 2018Article
- Kinin Receptors Sensitize TRPV4 Channel and Induce Mechanical Hyperalgesia: Relevance to Paclitaxel-Induced Peripheral Neuropathy in Mice.Molecular neurobiology · 2018Article
- Potentiation of Paclitaxel-Induced Pain Syndrome in Mice by Angiotensin I Converting Enzyme Inhibition and Involvement of Kinins.Molecular neurobiology · 2017Article
- Primary Role for Kinin BMolecular neurobiology · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeIn the current study, we investigated the role of both kinin B₁ and B₂ receptors in peripheral neuropathy induced by the chronic treatment of mice with paclitaxel a widely used chemotherapeutic agent. EXPERIMENTAL APPROACH: Chemotherapy-evoked hyperalgesia was induced by i.p. injections of paclitaxel (2 mg·kg⁻¹) over 5 consecutive days. Mechanical and thermal hyperalgesia were evaluated between 7 and 21 days after the first paclitaxel treatment. KEY
resultsTreatment with paclitaxel increased both mechanical and thermal hyperalgesia in mice (C57BL/6 and CD1 strains). Kinin receptor deficient mice (B₁, or B₂ receptor knock-out and B₁B₂ receptor, double knock-out) presented a significant reduction in paclitaxel-induced hypernociceptive responses in comparison to wild-type animals. Treatment of CD1 mice with kinin receptor antagonists (DALBK for B₁ or Hoe 140 for B₂ receptors) significantly inhibited both mechanical and thermal hyperalgesia when tested at 7 and 14 days after the first paclitaxel injection. DALBK and Hoe 140 were also effective against paclitaxel-induced peripheral neuropathy when given intrathecally or i.c.v. A marked increase in B₁ receptor mRNA was observed in the mouse thalamus, parietal and pre-frontal cortex from 7 days after the first paclitaxel treatment. CONCLUSIONS AND IMPLICATIONS: Kinins acting on both B₁ and B₂ receptors, expressed in spinal and supra-spinal sites, played a crucial role in controlling the hypernociceptive state caused by chronic treatment with paclitaxel.
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