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© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

We standardized a model by injecting Ehrlich tumor cells into the paw to evaluate cancer pain mechanisms and pharmacological treatments. Opioid treatment, but not cyclooxygenase inhibitor or tricyclic antidepressant treatments reduces Ehrlich tumor pain. To best use this model for drug screening it is essential to understand its pathophysiological mechanisms. Herein, we investigated the contribution of the transient receptor potential cation channel subfamily V member 1 (TRPV1) in the Ehrlich tumor-induced pain model. Dorsal root ganglia (DRG) neurons from the Ehrlich tumor mice presented higher activity (calcium levels using fluo-4 fluorescent probe) and an increased response to capsaicin (TRPV1 agonist) than the saline-injected animals (p < 0.05). We also observed diminished mechanical (electronic von Frey) and thermal (hot plate) hyperalgesia, paw flinching, and normalization of weight distribution imbalance in TRPV1 deficient mice (p < 0.05). On the other hand, TRPV1 deficiency did not alter paw volume or weight, indicating no significant alteration in tumor growth. Intrathecal injection of AMG9810 (TRPV1 antagonist) reduced ongoing Ehrlich tumor-triggered mechanical and thermal hyperalgesia (p < 0.05). Therefore, the contribution of TRPV1 to Ehrlich tumor pain behavior was revealed by genetic and pharmacological approaches, thus, supporting the use of this model to investigate TRPV1-targeting therapies for the treatment of cancer pain.

Details

Title
Ehrlich Tumor Induces TRPV1-Dependent Evoked and Non-Evoked Pain-like Behavior in Mice
Author
Bertozzi, Mariana M 1   VIAFID ORCID Logo  ; Saraiva-Santos, Telma 1 ; Zaninelli, Tiago H 1 ; Pinho-Ribeiro, Felipe A 2 ; Fattori, Victor 1 ; Staurengo-Ferrari, Larissa 1 ; Ferraz, Camila R 1   VIAFID ORCID Logo  ; Domiciano, Talita P 1 ; Calixto-Campos, Cassia 1 ; Borghi, Sergio M 3   VIAFID ORCID Logo  ; Zarpelon, Ana C 1 ; Cunha, Thiago M 4 ; Casagrande, Rubia 5   VIAFID ORCID Logo  ; Verri, Waldiceu A 1   VIAFID ORCID Logo 

 Laboratory of Pain, Inflammation, Neuropathy, and Cancer, Department of Pathology, Center of Biological Sciences, Londrina State University, Londrina 86057-970, PR, Brazil 
 Laboratory of Pain, Inflammation, Neuropathy, and Cancer, Department of Pathology, Center of Biological Sciences, Londrina State University, Londrina 86057-970, PR, Brazil; Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA 
 Laboratory of Pain, Inflammation, Neuropathy, and Cancer, Department of Pathology, Center of Biological Sciences, Londrina State University, Londrina 86057-970, PR, Brazil; Center for Research in Health Sciences, University of Northern Londrina, Londrina 86041-120, PR, Brazil 
 Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes, Ribeirão Preto 14049-900, SP, Brazil 
 Department of Pharmaceutical Sciences, Center of Health Science, Londrina State University, Londrina 86038-440, PR, Brazil 
First page
1247
Publication year
2022
Publication date
2022
Publisher
MDPI AG
e-ISSN
20763425
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2716504305
Copyright
© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.