| dc.description.abstract | In this study, we determined the therapeutic efect 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 efect
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 efective 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 | tr |
