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Öğe Analgesic Effects of Vilazodone, Indatraline, and Talsupram in a Rat Model of Neuropathic Pain(Galenos Publ House, 2022) Hacisuleyman, Levent; Sarac, Bulent; Joha, ZiadObjectives: Drugs that inhibit the reuptake of serotonin, norepinephrine, and/or dopamine are widely used for treating depressive disorders and have emerged as effective drugs for neuropathic pain. They have no substantial anti-nociceptive effects but are considered, with gabapentin/ pregabalin, first-line drugs for neuropathic pain. Materials and Methods: In this study, three different antidepressant agents were used in different doses to investigate their anti-hyperalgesic effects in rat models of neuropathic pain using hot plate and tail flick methods. They have different mechanisms of action; vilazodone hydrochloride is a selective serotonin inhibitor and a 5-HT1A partial agonist; talsupram hydrochloride is a selective noradrenaline inhibitor, and it has a high affinity for noradrenaline transporter (NET), whereas indatraline hydrochloride is a triple reuptake inhibitor that inhibits transporters for 5-HT (SERT), dopamine (DAT), and NET. Results: All the drugs used in the experiment were found to have an anti-hyperalgesic effect in both tests compared to the sham group. When antihyperalgesic effects of the three agents were compared to each other, it was found that talsupram hydrochloride was significantly more effective than the two other drugs in hot plate test. However, there was no statistically significant difference in the tail flick test. Indatraline hydrochloride was more effective than vilazodone hydrochloride at the same doses in the tail flick test. Conclusion: Our data suggest that three drugs are effective analgesics in rat models of neuropathic pain and inhibition of noradrenaline reuptake represents the cornerstone of analgesic mechanisms of effective antidepressants.Öğe Anticancer activity of lycopene in HT-29 colon cancer cell line(Humana Press Inc, 2023) Ataseven, Dilara; Ozturk, Aysegul; Ozkaraca, Mustafa; Joha, ZiadAn inverse association between serum lycopene levels and the risk of cancers has been pointed out by many prospective and retrospective epidemiological studies which prompted more studies to be performed on animal models and cell cultures in order to test this hypothesis. The aim of the present study was to evaluate the antiproliferative and pro-apoptotic effect of lycopene on colon cancer HT-29 cell line. The effect of lycopene on the viability of HT-29 cell line was investigated using XTT assay. The levels of Bcl-2, cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG in lycopene-treated HT-29 cells were measured using ELISA. Gamma-H2AX and cytochrome c expression was assessed semi-quantitatively using immunofluorescence staining. Lycopene at doses of 10 and 20 mu M produced a significant antiproliferative effect on HT-29 cells compared to the control (p < 0.05). The IC50 value of lycopene in HT-29 cells was found to be 7.89 mu M for 24 h. Lycopene (7.89 mu M) significantly elevated cleaved caspase 3 (p < 0.01), BAX, and cleaved PARP, 8-oxo-dG levels (p < 0.05). The levels of gamma-H2AX foci are significantly higher while the levels of cytochrome-c are lower (p < 0.05) in lycopene-treated HT-29 cells. These results indicate that lycopene has an antiproliferative apoptotic and genotoxic effect on HT-29 colon cancer cell line.Öğe Anticancer activity of lycopene in HT?29 colon cancer cell line(Mart 2023) Ataseven, Dilara; Öztürk, Ayşegül; Özkaraca, Mustafa; Joha, ZiadAn inverse association between serum lycopene levels and the risk of cancers has been pointed out by many prospective and retrospective epidemiological studies which prompted more studies to be performed on animal models and cell cultures in order to test this hypothesis. The aim of the present study was to evaluate the antiproliferative and pro-apoptotic efect of lycopene on colon cancer HT-29 cell line. The efect of lycopene on the viability of HT-29 cell line was investigated using XTT assay. The levels of Bcl-2, cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG in lycopene-treated HT-29 cells were measured using ELISA. Gamma-H2AX and cytochrome c expression was assessed semi-quantitatively using immunofuores cence staining. Lycopene at doses of 10 and 20 μM produced a signifcant antiproliferative efect on HT-29 cells compared to the control (p < 0.05). The IC50 value of lycopene in HT-29 cells was found to be 7.89 μM for 24 h. Lycopene (7.89 μM) signifcantly elevated cleaved caspase 3 (p < 0.01), BAX, and cleaved PARP, 8-oxo-dG levels (p < 0.05). The levels of γ-H2AX foci are signifcantly higher while the levels of cytochrome-c are lower (p < 0.05) in lycopene-treated HT-29 cells. These results indicate that lycopene has an antiproliferative apoptotic and genotoxic efect on HT-29 colon cancer cell lineÖğe Bromelain Protects Against PTZ-Induced Glial Damage and Inflammation: An In Vitro and In Silico Study(Humana Press Inc, 2025) Joha, Ziad; Basgoz, Neslihan; Ozgur, Aykut; Taskiran, Ahmet SevkiThis study aimed to investigate how bromelain protects glial cells from pentylenetetrazole (PTZ)-induced damage, focusing on its anti-inflammatory effects. C6 glioma cells were treated with PTZ, bromelain, or a combination of PTZ and bromelain. The interactions of bromelain with iNOS (Inducible Nitric Oxide Synthase) and COX2 (Cyclooxygenase-2) were investigated using molecular docking calculations. Cell viability was measured using the XTT (Methoxynitrosulfophenyl-Tetrazolium Carboxanilide) assay. iNOS, NO (Nitric Oxide), and COX2 levels were assessed using ELISA and immunofluorescence staining. Bromelain at 50 and 100 mu g/mL significantly increased cell viability (p < 0.001). On the other hand, bromelain at 50 g/mL reduced inflammation, as indicated by lower levels of NO, iNOS, and COX2 (p < 0.001). In-silico predictions suggest that bromelain can effectively target iNOS and COX2, key inflammatory proteins. These findings indicate that bromelain protects glial cells by exerting anti-inflammatory effects. However, further research is needed to understand the underlying mechanisms fully.Öğe Enoxaparin Protects C6 Glioma Cells from Glutamate-Induced Cytotoxicity by Reducing Oxidative Stress and Apoptosis(Springer, 2025) Yulak, Fatih; Joha, Ziad; Ozturk, Aysegul; Inan, Zeynep Deniz Sahin; Taskiran, Ahmet SevkiRecent studies suggest enoxaparin may protect the central nervous system (CNS) from damage. However, its specific effects on glial cells and the underlying mechanisms involving cell death and oxidative stress require further investigation. Therefore, this research investigated enoxaparin's potential to safeguard C6 glioma cells against glutamate-induced cytotoxicity, specifically focusing on its influence on oxidative stress and apoptotic mechanisms. To investigate the neuroprotective effects of enoxaparin against glutamate-induced cytotoxicity in C6 cells, four groups were established: a control group, a group exposed to 10 mM glutamate, a group treated with enoxaparin at concentrations ranging from 25 to 200 mu M, and a group receiving both 10 mM glutamate and enoxaparin at concentrations ranging from 25 to 200 mu M. Cell viability was measured using an XTT assay. To evaluate the effects of enoxaparin on oxidative stress, superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured using ELISA, along with total antioxidant status (TAS) and total oxidant status (TOS). Apoptosis was evaluated using flow cytometry, and caspase-3 activity, a key marker of apoptosis, was assessed using caspase-3 immunofluorescence staining. Enoxaparin at 50, 100, and 200 mu M markedly increased cell viability in the enoxaparin + glutamate group. Enoxaparin treatment in the enoxaparin + glutamate group also significantly elevated levels of SOD and TAS, while concurrently decreasing MDA and TOS levels. These changes indicate a reduction in oxidative stress. Enoxaparin treatment further resulted in a significant decline in cleaved caspase-3 levels, a marker of apoptosis. Enoxaparin pre-treatment reduced cell death according to flow cytometry analysis. This study suggests enoxaparin's potential to shield C6 glioma cells from glutamate-induced cell death by mitigating both oxidative stress and apoptotic pathways. More research is needed to confirm this effect.Öğe Ferroptosis inhibitor ferrostatin-1 attenuates morphine tolerance development in male rats by inhibiting dorsal root ganglion neuronal ferroptosis(Korean Pain Soc, 2024) Dirik, Hasan; Taskiran, Ahmet Sevki; Joha, ZiadBackground: Ferrostatin-1 and liproxstatin-1, both ferroptosis inhibitors, protect cells. Liproxstatin-1 decreases morphine tolerance. Yet, ferrostatin-1's effect on morphine tolerance remains unexplored. This study aimed to evaluate the influence of ferrostatin-1 on the advancement of morphine tolerance and understand the underlying mechanisms in male rats. Methods: This experiment involved 36 adult male Wistar albino rats with an average weight ranging from 220 to 260 g. These rats were categorized into six groups: Control, single dose ferrostatin-1, single dose morphine, single dose ferrostatin-1 + morphine, morphine tolerance (twice daily for five days), and ferrostatin-1 + morphine tolerance (twice daily for five days). The antinociceptive action was evaluated using both the hot plate and tail-flick tests. After completing the analgesic tests, tissue samples were gathered from the dorsal root ganglia (DRG) for subsequent analysis. The levels of glutathione, glutathione peroxidase 4 (GPX4), and nuclear factor erythroid 2-related factor 2 (Nrf2), along with the measurements of total oxidant status (TOS) and total antioxidant status (TAS), were assessed in the tissues of the DRG. Results: After tolerance development, the administration of ferrostatin-1 resulted in a significant decrease in morphine tolerance (P < 0.001). Additionally, ferrostatin-1 treatment led to elevated levels of glutathione, GPX4, Nrf2, and TOS (P < 0.001), while simultaneously causing a decrease in TAS levels (P < 0.001). Conclusions: The study found that ferrostatin-1 can reduce morphine tolerance by suppressing ferroptosis and reducing oxidative stress in DRG neurons, suggesting it as a potential therapy for preventing morphine tolerance.Öğe Investigation of the Analgesic Properties L-759,633 and SER 601 in Experimental Neuropathic Pain Model in Rats and their Comparison with Pregabalin(2023) Joha, Ziad; Yıldırım, Sahın; Hacısüleyman, Levent; Taşkıran, Ahmet ŞevkiDespite the fact that narcotics and NSAIDs are the mainstays of nociceptive pain care, only a small proportion of neuropathic pain patients benefit from them. Cannabinoid agents could be a viable alternative to opioids in the management of chronic pain. The goal of our investigation was to assess the analgesic efficacy of SER 601 and L-759,633, cannabinoid receptor 2 (CB2) agonists, at various doses in a model of neuropathic pain generated in rat. The analgesic effect of CB2 agonists L-759,633 and SER 601 at various doses in a rat model of neuropathic pain created by partial sciatic nerve ligation was examined by the hot plate method. Furthermore, a comparison of analgesic effects of both drugs with pregabalin is also conducted. The two substances demonstrated a dose-dependent analgesic effect in this model. The analgesic response of SER601 and L-759,633 in the neuropathic pain model was higher compared to that of pregabalin. All in all, our data suggest that SER601 and L-759,633 may offer a beneficial treatment option for neuropathic pain in future.Öğe Investigation of the effect of sugammadex on glutamate-induced neurotoxicity in C6 cell line and the roles played by nitric oxide and oxidative stress pathways(Wiley, 2023) Dirik, Hasan; Joha, ZiadThis experiment was intended to evaluate the effect of sugammadex on the cytotoxicity induced by glutamate, involving the nitric oxide and oxidative stress pathways. C6 glioma cells were used in the study. Glutamate was given to cells in the glutamate group for 24 h. Sugammadex at different concentrations was given to cells in the sugammadex group for 24 h. Cells in the sugammadex + glutamate group were pre-treated with sugammadex at various concentrations for 1 h and then exposed to glutamate for 24 h. XTT assay was used to assess cell viability. Levels of nitric oxide (NO), neuronal nitric oxide synthase (nNOS), total antioxidant (TAS), and total oxidant (TOS) in the cells were calculated using commercial kits. Apoptosis was detected by TUNEL assay. Sugammadex at concentrations of 50 and 100 mu g/mL significantly enhanced the cell viability in C6 cells after the cytotoxicity induced by glutamate (p < 0.001). Moreover, sugammadex considerably decreased the levels of nNOS NO and TOS and the number of apoptotic cells and increased the level of TAS (p < 0.001). Sugammadex has protective and antioxidant properties on cytotoxicity and could be an effective supplement for neurodegenerative diseases such as Alzheimer and Parkinson if further research in vivo supports this claim.Öğe Lycopene induces antiproliferative effects through apoptosis, autophagy, and oxidative DNA damage in the HeLa cells(Taylor & Francis Ltd, 2024) Parlak, Mesut; Joha, Ziad; Yulak, Fatih; Mendil, Ali Sefa; Tastemur, YasarBackground: This study explores the role of apoptosis, autophagy, and oxidative DNA damage in influencing the cytotoxic impact of lycopene on HeLa cells. Material and methods: Cell viability following exposure to varying lycopene concentrations was determined using an XTT assay. ELISA measured key cell death proteins (Bax, BCL-2, etc.), while immunofluorescence staining visualized LC3 beta (autophagy) and 8-oxo-dG (DNA damage). Results: Lycopene significantly killed HeLa cells in a dose-dependent way (IC50 = 10 mu M). Subsequent examinations conducted with the IC50 dose of lycopene demonstrated a notable elevation in the expression levels of apoptotic proteins, such as cleaved caspase 3, cleaved PARP, and Bax (p < 0.001). Additionally, treatment with this substance led to an increase in the levels of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicative of oxidative DNA damage. Furthermore, a significant rise (p < 0.05) in LC3 beta protein levels, a well-established indicator of autophagy activation, was noted. Conclusion: This study suggests lycopene's potential to fight cervical cancer by triggering programmed cell death (apoptosis) and cellular self-digestion (autophagy). These findings highlight lycopene as a promising candidate for future cervical cancer treatments.Öğe Mechanism of anti-cancer effect of ?-glucan on SH-SY5Y cell line(Bangladesh Pharmacological Soc, 2021) Filiz, Ahmet Kemal; Joha, Ziad; Yulak, FatihAnti-cancer property of fungi derived 13-glucan (Lentinula edodes) on several cancer cell lines have been reported. In this work, the SH-SY5Y cell lines were treated with various concentrations of 13-glucan (62.5, 125, 250 and 500 pg/mL) and the viability of the cells was tested using the XTT assay after 24 hours. Cleaved PARP, BCL-2, 8-hydroxy-desoxyguanosine (8-oxo-dG), cleaved caspase 3, Bax, total oxidant, and total antioxidant levels in the cells were measured by commercial kits. 13-Glucan significantly decreased the cell viability in SH-SY5Y cells. ELISA tests demonstrated that 13-glucan therapy dramatically increased 8-oxo-dG, cleaved caspase 3, Bax, cleaved PARP, total oxidant. However, 13-glucan treatment did not change the BCL-2 protein level. Altogether, 13-glucan caused significant cytotoxicity in SH-SY5Y cells by inducing oxidative stress, increasing DNA damage, and ultimately increasing apoptosis.Öğe Mechanism of anticancer effect of ETP-45658, a PI3K/AKT/mTOR pathway inhibitor on HT-29 Cells(Humana Press Inc, 2023) Yulak, Fatih; Filiz, Ahmet Kemal; Joha, Ziad; Ergul, MustafaThe PI3K pathway plays a crucial role in tumor cell proliferation across various cancers, including colon cancer, making it a promising treatment target. This study aims to investigate the antiproliferative activity of ETP-45658, a PI3K/AKT/mTOR pathway inhibitor, on colon cancer and elucidate the underlying mechanisms. HT-29 colon cancer cells were treated with varying doses of ETP 45658 and its cytotoxic effect assessed using the XTT cell viability assay.ELISA was also used to measure TAS, TOS, Bax, BCL-2, cleaved caspase 3, cleaved PARP, and 8-oxo-dG levels. Flow cytometry was performed to investigate apoptosis, cell cycle, caspase 3/7 activity, and mitochondrial membrane potential. Additionally, following the administration of DAPI (4,6-diamidino-2-phenylindole) dye, the cells were visualized using an immunofluorescence microscope. It was observed that ETP-45658 exerted a dose-dependent and statistically significant antiproliferative effect on HT-29 colon cancer cells. Further investigations using the IC50 dose showed that ETP-45658 decreased TAS levels and increased TOS levels and revealed that it upregulated apoptotic proteins while downregulating anti-apoptotic proteins. Our findings also showed that it increased Annexin V binding, arrested the cell cycle at G0/G1 phase, induced caspase 3/7 activity, impaired mitochondrial membrane potential, and ultimately triggered apoptosis in HT-29 cells. ETP-45658 shows promise against colon cancer by inducing cell death, and oxidative stress, and arresting the cell cycle. Targeting the PI3K/AKT/mTOR pathway with ETP-45658 offers exciting potential for colon cancer treatment.Öğe Mechanism of anticancer effect of gambogic acid on gastric signet ring cell carcinoma(Humana Press Inc, 2023) Joha, Ziad; Ozturk, Aysegul; Yulak, Fatih; Karatas, Ozhan; Ataseven, HilmiGambogic acid has demonstrated inhibitory effects on the growth of various cancer cell types, such as breast cancer, pancreatic cancer, prostate cancer, lung cancer, and osteosarcoma. This study aims to investigate the antiproliferative activity of Gambogic acid on SNU-16 cells derived from gastric signet ring cell carcinoma and elucidate the underlying mechanisms. The cytotoxic effect of gambogic acid was evaluated in SNU-16 cells by treating them with different concentrations of the compound, and the XTT cell viability assay was employed to assess cell viability. ELISA was used to measure bax, BCL-2, caspase 3, PARP, and 8-oxo-dG levels. Additionally, immunofluorescence staining was applied to assess 8-oxo-dG and LC3 & beta; levels in SNU-16 cells. It was observed that gambogic acid exerted a dose-dependent and statistically significant antiproliferative effect on SNU-16 cells. The IC50 value of gambogic acid in SNU-16 cells was found to be 655.1 nM for 24 h. Subsequent investigations conducted using the IC50 dose revealed a significant upregulation of apoptotic proteins including cleaved caspase 3, Bax, and cleaved PARP (p < 0.001), along with a downregulation of BCL-2 (p < 0.001), an anti-apoptotic protein. Moreover, the administration of this drug led to an upregulation of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicating oxidative damage in DNA, as well as an increase in LC3 & beta; levels (p < 0.05), a marker associated with autophagy. The antiproliferative effect of gambogic acid against gastric signet ring cell carcinoma is attributed to its ability to induce apoptosis and autophagy. This discovery highlights the promising potential of gambogic acid as a treatment option for gastric signet ring cell carcinoma.Öğe Protective Effect of Astaxanthin Against Oxidative Stress-Induced Apoptosis and Inflammatory Increase in C6 Cells Induced by Hydrogen Peroxide(2023) Joha, Ziad; Taşkıran, Ahmet ŞevkiRecent findings have indicated the potential protective impacts of astaxanthin on the central nervous system (CNS). Nevertheless, the precise influence of astaxanthin on oxidative damage caused by hydrogen peroxide (H2O2) in glial cells, as well as its interplay with apoptotic and inflammatory mechanisms, remain unclear. As a result, the primary goal of this study was to explore how astaxanthin functions as a safeguard against glial cell damage induced by oxidative stress triggered by H2O2, particularly focusing on its involvement in inflammatory and apoptotic pathways. The study employed C6 glioma cells as the experimental model. Cells in the H2O2 group were subjected to hydrogen peroxide (H2O2) treatment for 24 hours. In the astaxanthin group, cells were treated with varying concentrations of astaxanthin for 24 hours. For the astaxanthin + H2O2 group, cells were first pre-treated with different concentrations of astaxanthin for 1 hour and subsequently exposed to H2O2 for 24 hours. The XTT assay was utilized to evaluate cell viability. To demonstrate the antioxidative effect, total oxidant status (TOS) and total antioxidant status (TAS) measurements were conducted TNF-? and IL-1? levels were assessed using the ELISA method to measure anti-inflammatory effect. ELISA was also employed to measure the anti-apoptotic effect, involving the measurement of caspase 3, BAX, and Bcl-2 levels. In the group treated with both astaxanthin and H2O2, astaxanthin exhibited a notable increase in cell viability within C6 cells. Additionally, it significantly elevated the levels of TAS while decreasing the levels of TOS, indicative of reduced oxidative stress. Furthermore, astaxanthin demonstrated a significant reduction in inflammatory markers, including TNF-? and IL-1? levels. Moreover, it led to a substantial decrease in apoptotic markers, specifically cleaved caspase-3 and Bax, while simultaneously increasing the levels of the anti-apoptotic protein Bcl-2. Astaxanthin demonstrates protective properties by engaging anti-inflammatory and anti-apoptotic pathways, countering the oxidative stress induced by hydrogen peroxide in C6 glioma cells. However, a more comprehensive investigation is required to address the potential underlying mechanisms.Öğe The Role of Nitric Oxide Pathway in the Anti-Epileptogenic Effect of Valproic Acid in the Pentylenetetrazole-Kindling Model in Rats(Maik Nauka/Interperiodica/Springer, 2023) Sahin, Bilal; Filiz, Ahmet Kemal; Joha, ZiadThough valproic acid (VPA) is used to treat seizures, more investigations have been needed to understand the effect of VPA on the nitric oxide pathway in epilepsy. Our investigation aimed to study the effect of VPA on cortical and hippocampal NOS isomers in epileptogenesis processes in the PTZ kindling model of epilepsy in the rat to reveal its mechanisms of action. Twenty-four male Wistar albino rats were used in this study. The animals were divided into four groups control, PTZ without VPA, and PTZ with VPA at two doses (100 and 200 mg/kg) Rats were kindled by injections of PTZ (35 mg/kg) with drugs or vehicle 30 minutes before, once every other day for 12 times and their behavior was observed. After completing the epileptic model process, nitric oxide pathway markers (eNOS, nNOS, iNOS, and NO) in the cortex and hippocampus were assessed by using ELISA methods. VPA suppressed seizure stages and decreased nNOS, iNOS, and NO levels while increasing eNOS levels in the hippocampus and cerebral cortex. The effect of VPA on nitric oxide pathway was found to contribute to its anti-epileptic activity.
