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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 Antimicrobial, anti-biofilm and cytotoxic properties of methallyl functionalized benzimidazolium-derived Ag(I)-N- heterocyclic carbene complexes(Pharmacotherapy Group, 2022) Celik, Cem; Tutar, Ugur; Sahin, Neslihan; Ozturk, AysegulPurpose: To investigate the antimicrobial, antibiofilm, and cytotoxicity properties of methallyl substituted benzimidazolium-based, silver-bound N-heterocyclic carbene (Ag(I)-NHC) complexes, with respect to their potential to act as antimicrobial agents. Methods: The antimicrobial, antibiofilm, and cytotoxicity properties of the four complexes, the synthesis and characterization of which were carried out previously, were investigated. The antimicrobial properties were tested using the broth microdilution method, while their antibiofilm potential were determined by microtiter plate assay. The L-929 cell line was used for cytotoxic studies. Results: Strong antibiofilm and antimicrobial effects were produced by Ag(I)-NHC complexes. Compounds 2 and 3 showed potent activities against E. coli strain, with effects similar to that of positive control antibiotic, while compounds 1 and 4 exhibited antimicrobial activity at a concentration of 31.2 mu g/mL. The compounds were effective against biofilms formed at concentrations in the range of 32 - 84 %, and degraded mature biofilms at a concentration range of 14 -66 %. Compounds 1 and 2 did not significantly affect cell survival (p > 0.05), while compounds 3 and 4 significantly reduced cell survival, when compared with untreated cells in the control group (p < 0.001). Conclusion: This study may be one of the few studies on benzimidazolium-derived NHCs. The compounds which produced antimicrobial, antibiofilm, and cytotoxic properties in this study may be valuable and novel antimicrobial agents. Therefore, there is need for further in vivo and in vitro studies on these compounds.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 HER-2 SMASH (vol 95, 10, 2025)(Springer, 2025) Alandag, Celal; Ozturk, Aysegul; Yulak, Fatih; Sahin Inan, Zeynep Deniz; Ozkaraca, Mustafa; Lacin, Burak Batuhan; Altun, Ahmet[No abstract available]Öğe Inhibition of the TRPM2 cation channel attenuates morphine tolerance by modulating endoplasmic reticulum stress and apoptosis in rats(Elsevier Ireland Ltd, 2025) Ciltas, Arzuhan Cetindag; Ozdemir, Ercan; Gunes, Handan; Ozturk, AysegulOpioid drugs such as morphine are frequently preferred drugs for severe pain in cancer and chronic diseases, but long-term use causes opioid tolerance. The mechanism of tolerance to opioids is quite complex and not fully understood. Our aim in this study was to investigate the effects of TRPM2 cation channel antagonists N-(pamylcinnamoyl) anthranilic acid (ACA) and 2-aminoethoxydiphenyl borate (2-APB) on morphine analgesia and tolerance in rats. Forty-eight Wistar Albino male rats were included in the study and the rats were randomly divided into drug and control (saline) groups. To induce morphine tolerance, the rats were injected with 10 mg/ kg morphine intraperitoneally for 7 days. After thermal analgesia tests, dorsal root ganglion (DRG) and cortex tissues were isolated. Proapoptotic mediators caspase-3 and 9, total oxidant status (TOS) and total antioxidant status (TAS) and ER stress proteins GRP78/BiP, ATF-6, p-IRE1 and pERK levels were measured by biochemical analysis of tissue homogenates. The findings showed that there was a significant decrease in morphine tolerance in rats administered ACA and 2-APB (p<0.05). In addition, biochemical tests revealed a significant decrease in ER stress proteins, proapoptotic biomarkers and TOS levels and a significant increase in TAS levels in DRG, thalamus and sensory cortex tissues (p<0.05). In conclusion, inhibition of TRPM2 cation channel by ACA and 2APB reduces morphine tolerance by preventing ER stress and apoptosis. It may be possible to increase the analgesic potential of morphine by combined application with ACA and 2-APB in the clinic, but further experimental and molecular studies are needed.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 Positive effects of angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole-induced epileptic seizures in mice(Pharmacotherapy Group, 2020) Tastemur, Yasar; Gumus, Erkan; Ergul, Merve; Ulu, Mustafa; Akkaya, Recep; Ozturk, Aysegul; Taskiran, Ahmet SevkiPurpose: To evaluate the effects of an angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole (PTZ)-induced seizures and post-seizure hippocampal injury. Materials: Thirty-five male Balb-c mice weighing 30 - 33 g were divided into control, saline PTZ, s(erum ;physiologic 1 ml/kg as solvent), positive control (valproic acid 200 mg/kg), captopril (25 mg/kg/day for 7 days), and captopril (50 mg/kg/ day for 7 days) groups. PTZ (60 mg/kg) was administered thirty minutes after medication administration to induce epileptic seizures. The animals were observed for 30 min to record Racine stages, the time of the first myoclonic jerk (FMJ), and the occurrence of the first generalized tonic-clonic seizure (GTCS). Cornu Ammonis (CA)1, CA2, CA3, and the dentate gyrus (DG) of the hippocampus underwent histopathological examinations. The levels of total oxidant status (TOS), oxidative stress markers (total antioxidant status, TAS), and oxidative stress index (OSI) were measured in the brain tissue. Results: Compared to PTZ group, 25 mg/kg captopril decreased seizure scores and delayed FMJ and GTCS (p < 0.05). Histopathological assessment demonstrated that both 25 and 50 mg/kg captopril alleviated neuronal injury in CA1, CA2, CA3, and DG compared to PTZ (p < 0.05). Also, TOS and OSI levels in the brain tissue were reduced by both 25 and 50 mg/kg doses of captopril (p < 0.05). Conclusion: Captopril favorably improves epileptic seizure parameters and acts against post-seizure neuronal injury in the hippocampus. Captopril may be a drug of choice in epileptic individuals with hypertension.Öğe Sinapic acid alleviates glutamate-induced excitotoxicity by inhibiting neuroinflammation and endoplasmic reticulum stress pathway in C6 glioma cells(Pergamon-Elsevier Science Ltd, 2025) Ortasoz, Ahmet Mahmut; Ozdemir, Ercan; Taskiran, Ahmet Sevki; Ozturk, AysegulSinapic acid (SA) is a polyphenol compound derived from hydroxycinnamic acid found in various foods such as cereals and vegetables and has antioxidant, anti-inflammatory and neuroprotective properties. However, its effects on glutamate-induced excitotoxicity, which is important in neurodegenerative diseases, have not been fully elucidated. This study aimed to investigate the effect of SA on glutamate excitotoxicity and the possible role of proinflammatory cytokines and the endoplasmic reticulum (ER) stress pathway. In the study, C6 rat glioma cell line was used and the cells were divided into 4 groups: control, glutamate, SA and glutamate+SA. Cells were treated with 10 mM glutamate for 24 h to induce excitotoxicity. Additionally, SA was applied to cells at concentrations of 12.5 to 100 mu M to examine its effects on glutamate excitotoxicity. XTT test was used for cell viability, and apoptotic cells were determined by immunofluorescence and flow cytometry methods. Proinflammatory cytokines (tumor necrosis factor-alpha, TNF-alpha and interleukin-beta, IL-1(3), ER stress markers (glucose regulatory protein 78, GRP78; C/EBP homologous protein, CHOP and activating transcription factor-4, ATF-4) and caspase-3 was used to measure ELISA method. Findings indicated that SA (50 mu M) significantly increased cell viability against glutamate-induced excitotoxicity (p < 0.05). Also, SA caused a significant decrease in TNF-alpha, IL-1(3, GRP78, CHOP, ATF-4 and caspase-3 levels in glutamate-treated cells (p < 0.05). Flow cytometry and immunofluorescence staining results showed that SA reduced apoptosis in C6 glioma cells. In conclusion, our findings suggested that SA attenuated glutamate-induced excitotoxicity by preventing apoptosis through reducing proinflammatory cytokines and ER stress protein levels.Öğe The Effects of Proton Pump Inhibitors (Pantoprazole) on Pentylenetetrazole-Induced Epileptic Seizures in Rats and Neurotoxicity in the SH-SY5Y Human Neuroblastoma Cell Line(Springer/Plenum Publishers, 2021) Taskiran, Ahmet Sevki; Ergul, Mustafa; Gunes, Handan; Ozturk, Aysegul; Sahin, Bilal; Ozdemir, ErcanRecent studies have shown that proton pump inhibitors have positive effects on the nervous system. However, its effect on epileptic seizure and neuronal damage are still unclear. In this study, it was aimed to investigate the effect of pantoprazole on pentylenetetrazole-induced epileptic seizures in rats and neurotoxicity in the SH-SY5Y cell line. Animals were divided into three groups: control, saline (1 mL/kg serum physiologic), and pantoprazole (10 mg/kg). Pentylenetetrazole (45 mg/kg) was given to induce a seizure and a passive avoidance test trial was carried out to evaluate memory function. 8-hydroxy-2 '-deoxyguanosine (8-OHdG), caspase-3, and brain-derived neurotrophic factor (BDNF) levels were measured in the brain by commercial kits. SH-SY5Y cells were treated with saline or pantoprazole for one hour, and then pentylenetetrazole (30 mu m) was added to the medium to induce neurotoxicity. After 24 h, cell viability, total antioxidant, total oxidant status, and apoptosis were measured in SH-SY5Y cells. It was found that pantoprazole treatment postponed epileptic seizure onset, protected memory, reduced 8-OHdG, caspase-3, and also increased BDNF in the brain. In addition, it blocked pentylenetetrazole toxicity, apoptosis, increased antioxidant, and decreased oxidant status in SH-SY5Y cells. Pantoprazole significantly improved seizure, oxidative stress, and apoptosis. Thus, pantoprazole could be used as a supportive therapeutic agent in epilepsy.Öğe Unveiling the Protective Potential of Sugammadex against PTZ-Induced Epileptic Seizures in Mice: A Comprehensive Study on Oxidative Stress, Apoptosis, and Autophagy(Maik Nauka/Interperiodica/Springer, 2024) Karademir, Mustafa; Ozturk, Aysegul; Yulak, Fatih; Ozkaraca, Mustafa; Taskiran, Ahmet SevkiSugammadex (SUG) is a modified gamma-cyclodextrin molecule used in patients under general anesthesia to reverse the effects of neuromuscular blocking agents. Besides, recent studies have shown that SUG positively affects the nervous system. However, its effect on seizures is still unclear. The current study aimed to examine the effects of SUG on pentylenetetrazole (PTZ)-induced epileptic seizures in mice. The mice were randomly divided into four groups. Group 1 was controlled, group 2 was administered saline (1 mL/kg serum physiologic), and Groups 3 and 4 were administered Sugammadex (150 and 300 mg/kg). Pentylenetetrazole (60 mg/kg) was given to induce seizures 30 min after saline or drug administration except for the control group. Total oxidant status (TOS) and total antioxidant status (TAS) levels in the hippocampus and cortex were measured using a commercial kit. 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), 3,3 dityrosine, caspase-3, apoptosis-inducing factor (AIF), and light chain 3 (LC3B) levels in the hippocampal CA1 region and cortex after seizures were evaluated immunohistochemical staining. SUG reduced seizure stages and increased epileptic seizure onset times. Moreover, it decreased TOS levels and increased TAS levels in the hippocampus and cortex. Besides, after seizures, it reduced 4-HNE, 3,3 dityrosandine, caspase-3, and LC3B immunohistochemical scores in the hippocampal CA1 region and cortex. SUG has protective effects on pentylenetetrazole-induced seizures in mice, alleviating seizures, oxidative stress, apoptosis, and autophagy. The anticonvulsant mechanism of SUG may be related to the inhibition of the oxidative stress pathway.
