Parthenolide as a potential analgesic in the treatment of paclitaxel-induced neuropathic pain: the rat modeling

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dc.authoridBayram, Cemil/0000-0001-8940-8560
dc.contributor.authorToraman, Emine
dc.contributor.authorBayram, Cemil
dc.contributor.authorSezen, Selma
dc.contributor.authorOzkaraca, Mustafa
dc.contributor.authorHacimuftuoglu, Ahmet
dc.contributor.authorBudak, Harun
dc.date.accessioned2024-10-26T18:09:00Z
dc.date.available2024-10-26T18:09:00Z
dc.date.issued2023
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractIn this study, we determined the therapeutic effect of parthenolide (PTL), the active component of Tanacetum parthenium, on neuropathic pain caused by paclitaxel (PTX), a chemotherapeutic drug frequently used in cancer treatment, at the gene and protein levels. To this end, 6 groups were formed: control, PTX, sham, 1 mg/PTL, 2 mg/kg PTL, and 4 mg/kg PTL. Pain formation was tested by Randall-Selitto analgesiometry and locomotor activity behavioral analysis. Then, PTL treatment was performed for 14 days. After the last dose of PTL was taken, Hcn2, Trpa1, Scn9a, and Kcns1 gene expressions were measured in rat brain (cerebral cortex/CTX) tissues. In addition, changes in the levels of SCN9A and KCNS1 proteins were determined by immunohistochemical analysis. Histopathological hematoxylin-eosin staining was also performed to investigate the effect of PTL in treating tissue damage on neuropathic pain caused by PTX treatment. When the obtained data were analyzed, pain threshold and locomotor activity decreased in PTX and sham groups and increased with PTL treatment. In addition, it was observed that the expression of the Hcn2, Trpa1, and Scn9a genes decreased while the Kcns1 gene expression increased. When protein levels were examined, it was determined that SCN9A protein expression decreased and the KCNS1 protein level increased. It was determined that PTL treatment also improved PTX-induced tissue damage. The results of this study demonstrate that non-opioid PTL is an effective therapeutic agent in the treatment of chemotherapy-induced neuropathic pain, especially when used at a dose of 4 mg/kg acting on sodium and potassium channels.
dc.description.sponsorshipAtatuerk University Scientific Research Projects Coordination Commission [FDK-2020-8345]
dc.description.sponsorshipFinancial support for the present research was received from Atatuerk University Scientific Research Projects Coordination Commission [Grant Number: FDK-2020-8345].
dc.identifier.doi10.1007/s00210-023-02568-5
dc.identifier.endpage3721
dc.identifier.issn0028-1298
dc.identifier.issn1432-1912
dc.identifier.issue12
dc.identifier.pmid37306715
dc.identifier.scopus2-s2.0-85161641912
dc.identifier.scopusqualityQ2
dc.identifier.startpage3707
dc.identifier.urihttps://doi.org/10.1007/s00210-023-02568-5
dc.identifier.urihttps://hdl.handle.net/20.500.12418/29884
dc.identifier.volume396
dc.identifier.wosWOS:001007417400001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofNaunyn-Schmiedebergs Archives of Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectParthenolide
dc.subjectCancer
dc.subjectPaclitaxel-induced neuropathic pain
dc.subjectPaclitaxel
dc.subjectExpression
dc.subjectBioinformatics
dc.titleParthenolide as a potential analgesic in the treatment of paclitaxel-induced neuropathic pain: the rat modeling
dc.typeArticle

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