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    Evaluated periodontal tissues and oxidative stress in rats with neuropathic pain-like behavior
    (Ekim 2023) Toraman, Ayşe; Toraman, Emine; Özkaraca, Mustafa; Budak, Harun
    Background Oxidative stress has a critical effect on both persistent pain states and periodontal disease. Voltage-gated sodium NaV1.7 (SCN9A), and transient receptor potential ankyrin 1 (TRPA1) are pain genes. The goal of this study was to investi gate oxidative stress markers, periodontal status, SCN9A, and TRPA1 channel expression in periodontal tissues of rats with paclitaxel-induced neuropathic pain-like behavior (NPLB). Methods and results Totally 16 male Sprague Dawley rats were used: control (n=8) and paclitaxel-induced pain (PTX) (n=8). The alveolar bone loss and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were analyzed histometrically and immu nohistochemically. Gingival superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities (spectrophotometric assay) were measured. The relative TRPA1 and SCN9A genes expression levels were evaluated using quantitative real-time PCR (qPCR) in the tissues of gingiva and brain. The PTX group had significantly higher alveolar bone loss and 8-OHdG compared to the control. The PTX group had significantly lower gingival SOD, GPx and CAT activity than the control groups. The PTX group had significantly higher relative gene expression of SCN9A (p=0.0002) and TRPA1 (p=0.0002) than the control in gingival tissues. Increased nociceptive susceptibility may affect the increase in oxidative stress and periodontal destruction. Conclusions Chronic pain conditions may increase TRPA1 and SCN9A gene expression in the periodontium. The data of the current study may help develop novel approaches both to maintain periodontal health and alleviate pain in patients suffering from orofacial pain.
  • Küçük Resim Yok
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    Evaluated periodontal tissues and oxidative stress in rats with neuropathic pain-like behavior
    (Springer, 2023) Toraman, Ayse; Toraman, Emine; Ozkaraca, Mustafa; Budak, Harun
    Background Oxidative stress has a critical effect on both persistent pain states and periodontal disease. Voltage-gated sodium NaV1.7 (SCN9A), and transient receptor potential ankyrin 1 (TRPA1) are pain genes. The goal of this study was to investigate oxidative stress markers, periodontal status, SCN9A, and TRPA1 channel expression in periodontal tissues of rats with paclitaxel-induced neuropathic pain-like behavior (NPLB). Methods and results Totally 16 male Sprague Dawley rats were used: control (n=8) and paclitaxel-induced pain (PTX) (n=8). The alveolar bone loss and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were analyzed histometrically and immunohistochemically. Gingival superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities (spectrophotometric assay) were measured. The relative TRPA1 and SCN9A genes expression levels were evaluated using quantitative real-time PCR (qPCR) in the tissues of gingiva and brain. The PTX group had significantly higher alveolar bone loss and 8-OHdG compared to the control. The PTX group had significantly lower gingival SOD, GPx and CAT activity than the control groups. The PTX group had significantly higher relative gene expression of SCN9A (p=0.0002) and TRPA1 (p=0.0002) than the control in gingival tissues. Increased nociceptive susceptibility may affect the increase in oxidative stress and periodontal destruction. Conclusions Chronic pain conditions may increase TRPA1 and SCN9A gene expression in the periodontium. The data of the current study may help develop novel approaches both to maintain periodontal health and alleviate pain in patients suffering from orofacial pain.
  • Küçük Resim Yok
    Öğe
    Increased nociceptive sensitivity is associated with periodontal inflammation and expression of chronic pain genes in gingival tissues of male rats
    (Elsevier Ireland Ltd, 2022) Toraman, Ayse; Toraman, Emine; Ozkaraca, Mustafa; Budak, Harun
    Objective: This study aimed to evaluate the inflammatory response, hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2), and voltage-gated potassium (Kv) 9.1 channel expression in rats with paclitaxel-induced neuropathic pain-like behavior. Methods: Sixteen male Sprague Dawley rats were divided equally into two groups: control and paclitaxel-induced pain (PTX). The attachment loss and inflammatory cell infiltrate levels were analyzed histometrically and immunohistochemically. The gene expression of HCN2 and KCNS1 was analyzed by qPCR in the brain and gingival tissues. Results: The attachment loss and prominent infiltration of inflammatory cells were significantly higher in the PTX group than in the control groups. In gingival tissues; the expression levels of HCN2 (p = 0,0011) were significantly higher and KCNS1 (p = 0,0003) were significantly lower in the PTX group than in the control groups. Conclusion: Increased nociceptive sensitivity, may play a role in periodontal inflammation. KCNS1 may decrease and HCN2 expression may increase in periodontium in permanent chronic pain states. The results of the present study may be helpful in developing new approaches to alleviate pain and maintain periodontal health in patients suffering from orofacial pain.
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    Parthenolide as a potential analgesic in the treatment of paclitaxel?induced neuropathic pain: the rat modeling
    (Haziran 2023) Toraman, Emine; Bayram, Cemil; Sezen, Selma; Özkaraca, Mustafa; Hacımüftüoğlu, Ahmet; Budak, Harun
    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
  • Küçük Resim Yok
    Öğe
    Parthenolide as a potential analgesic in the treatment of paclitaxel-induced neuropathic pain: the rat modeling
    (Springer, 2023) Toraman, Emine; Bayram, Cemil; Sezen, Selma; Ozkaraca, Mustafa; Hacimuftuoglu, Ahmet; Budak, Harun
    In 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.