The effects of tramadol on cancer stem cells and metabolic changes in colon carcinoma cells lines

Özgürbüz, Uğur; Gencur, S.; Kurt, Feyzan Özdal; Özkalkanlı, Murat Yaşar; Vatansever, Hafize Seda

doi:10.1016/j.gene.2019.144030

Cited by 10 publications

(2 citation statements)

References 9 publications

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“…In contrast, Ozgurbuz et al demonstrated that tramadol hydrochloride significantly increased VEGF expression in specific colon cancer cell lines when compared to the control group. They suggested that tramadol hydrochloride might potentially influence angiogenic potential [22]. In our study, three different immunohistochemical vascular markers were used to evaluate angiogenesis, and the results were interpreted against tramadol hydrochloride.…”

Section: Discussionmentioning

confidence: 97%

Effects of systemically administered tramadol hydrochloride on random pattern skin flap survival in rats

Ors Yildirim,

Kadan,

Yildirim

et al. 2024

Turk J Vasc Surg

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Aim: Tramadol is a weak centrally acting opioid analgesic with µ-opioid receptor agonist effects. It has been explored for its analgesic efficacy through various in-vitro and in-vivo studies. The skin, as the body’s largest organ and the protector barrier, is vulnerable to injuries and wounds that can cause significant challenges due to pain, economic burdens and psychological implications. Successful healing of wound involves complex processes and it is influenced by factors such as angiogenesis and nitric oxide levels. This study investigates the effects of tramadol on wound healing in experimental ischemic wound models in rats. Material and Methods: Two 6 mm ischemic wound models were created on the backs of 30 male Wistar Albino rats, with wound areas cut along the long edges and a sterile silicone material placed between the panniculus carnosus fascia and paraspinosus muscle. Rats were randomized into Tramadol, Control, and Sham groups. The wounds were imaged using a "SONY ILCE-7" camera on days 0, 3, 6, 10, and 14. Wound areas and healing percentages were calculated from the images and recorded for statistical purposes. After 14 days, the animals were sacrificed under general anesthesia for histopathological examination of tissue samples. CD31 and VEGF antibodies were used to evaluate the density and morphology of vascular structures. Results: Tramadol administration accelerated the healing of wound surface area. Significant differences were found between groups in terms of inflammation, and data recorded in CD34, CD31, and VEGF-stained preparations. Conclusion: The study found that tramadol positively contributes to wound healing in the acute phase of ischemic wounds by affecting various processes.

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Section: Discussionmentioning

confidence: 97%

Effects of systemically administered tramadol hydrochloride on random pattern skin flap survival in rats

Ors Yildirim,

Kadan,

Yildirim

et al. 2024

Turk J Vasc Surg

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“…In addition, reduced expression of Ki-67 and Bcl-2 in HCT116 CD133 (+) and CD133 (−) cells. However, the authors showed that tramadol did not affect VEGF expression in HCT116 CD133(+) and CD133(−) cells, whereas, in the case of Colo320 and Colo741 CD133(+), it was increased compared with the control group [56].…”

Section: Opioids Impact Cell Cycle and Apoptosismentioning

confidence: 90%

Opioids in Cancer Development, Progression and Metastasis: Focus on Colorectal Cancer

Szczepaniak

Fichna

Zielińska

2020

Curr. Treat. Options in Oncol.

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Colorectal cancer I Endogenous opioid system I Opioid receptors I Opioids I Opium Abbreviations COX-2 cyclooxygenase-2. _ CRC colorectal cancer. _ DCs dendritic cells. _ DEN diethylnitrosamine. _ GPCR Gprotein-coupled receptors. _ IBD inflammatory bowel disease. _ IL-1β interleukin 1β. _ IL-6 interleukin 6. _ MMT methadone maintenance treatment. _ MOR mu opioid receptor. _ n-Cdh n-cadherin. _ NK natural killer cell. _ Nx propofol with epidural anesthesia. _ PGE2 prostaglandin E2. _ TJ tight junction. _ TLR toll-like receptor. _ TNFα tumor necrosis factor α. _ TPA 2-o-tetradecanoyl-phorbol-13-acetate. _ uPA urokinase plasminogen activator. _ ZO zonulaoccludens. Opinion statement So far, opioids have been successfully used to reduce cancer pain in patients in order to improve their quality of life. However, the use of opioids leads to numerous side effects such as constipation, drowsiness, nausea, itching, increased sweating and hormonal changes. In this review, we described the action of opioids in several molecular pathways significant for maintenance of the intestinal homeostasis including the impact on the intestinal epithelium integrity, changes in microbiome composition, modulation of the immune system or induction of apoptosis and inhibition of angiogenesis. We summed up the role of individual opioids in the processes involved in the growth and development of cancer and elucidated if targeting opioid receptors may constitute novel therapeutic option in colon cancer.

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Effect of tramadol on apoptosis and synaptogenesis in hippocampal neurons: The possible role of µ‐opioid receptor

Hosseindoost

Akbarabadi

Sadat‐Shirazi

et al. 2022

Drug Development Research

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Tramadol is a synthetic opioid with centrally acting analgesic activity that alleviates moderate to severe pain and treats withdrawal symptoms of the other opioids. Like other opioid drugs, tramadol abuse has adverse effects on central nervous system components. Chronic administration of tramadol induces maladaptive plasticity in brain structures responsible for cognitive function, such as the hippocampus. However, the mechanisms by which tramadol induces these alternations are not entirely understood. Here, we examine the effect of tramadol on apoptosis and synaptogenesis of hippocampal neuronal in vitro. First, the primary culture of hippocampal neurons from neonatal rats was established, and the purity of the neuronal cells was verified by immunofluorescent staining. To evaluate the effect of tramadol on neuronal cell viability MTT assay was carried out. The western blot analysis technique was performed for the assessment of apoptosis and synaptogenesis markers. Results show that chronic exposure to tramadol reduces cell viability of neuronal cells and naloxone reverses this effect. Also, the level of caspase‐3 significantly increased in tramadol‐exposed hippocampal neurons. Moreover, tramadol downregulates protein levels of synaptophysin and stathmin as synaptogenesis markers. Interestingly, the effects of tramadol were abrogated by naloxone treatment. These findings suggest that tramadol can induce neurotoxicity in hippocampal neuronal cells, and this effect was partly mediated through opioid receptors.

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The effects of tramadol on cancer stem cells and metabolic changes in colon carcinoma cells lines

Cited by 10 publications

References 9 publications

Effects of systemically administered tramadol hydrochloride on random pattern skin flap survival in rats

Effects of systemically administered tramadol hydrochloride on random pattern skin flap survival in rats

Opioids in Cancer Development, Progression and Metastasis: Focus on Colorectal Cancer

Effect of tramadol on apoptosis and synaptogenesis in hippocampal neurons: The possible role of µ‐opioid receptor

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