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    Agomelatine attenuates calcium signaling and apoptosis via the inhibition of TRPV1 channel in the hippocampal neurons of rats with chronic mild stress depression model
    (Elsevier B.V., 2022) Özdamar Ünal, Gülin; Demirdaş, Arif; Naziro?lu, Mustafa; Övey, İshak Suat
    Chronic stress plays a key role in inducing various clinical disorders through mechanistic pathways, including oxidative stress and apoptosis. Transient receptor potential vanilloid 1 (TRPV1) channels, which are permeable to cations, mainly Ca2+, are susceptible to oxidative stress. Agomelatine (AGOM) is an antidepressant drug analogous to the antioxidant melatonin hormone, although its action has not been fully clarified yet. We aimed to investigate the protective role of AGOM on TRPV1-induced Ca2+ signaling and apoptosis in rats with chronic mild stress (CMS). The rats were divided into six main groups: control, dimethyl sulfoxide (DMSO), AGOM, CMS, CMS+DMSO, and CMS+AGOM. Five weeks of CMS were applied to rats in the CMS groups. The induction of CMS was confirmed with the sucrose preference test. The AGOM treatments were administered in the last three weeks of the experiment. The depression-like behavior, TRPV1-mediated cytosolic Ca2+ influx, lipid peroxidation, apoptosis, caspase ? 3, and ? 9 levels increased in the hippocampal neurons of CMS groups, although cell viability level was diminished by the CMS exposure. However, AGOM treatment downregulated stress-related behaviors, hippocampal oxidant and apoptotic markers by modulating the TRPV1 activity. In conclusion, TRPV1-mediated Ca2+ signaling and apoptosis may play a role in the etiopathogenesis of experimental depression. By regulating these changes with AGOM treatment, a positive contribution may be made to depression treatment. © 2022 Elsevier B.V.
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    Alzheimer Hastalığının Önlenmesi ve Tedavisinde Melatoninin TRPA1 Kanalları Üzerinden Potansiyel Etkileri
    (2022) Özşimşek, Ahmet; Övey, İshak Suat
    Amaç: Alzheimer hastalığı (AH) demansın en yaygın nedenidir ve ilerleyici bir nörodejeneratif hastalık olarak tanımlanır. AH ilerleyici bozukluğunun ana klinik özellikleri öğrenme ve hafıza kaybıdır. Çeşitli çalışmalar mitokondrinin AH patogenezinde kritik bir rol oynadığını göstermiştir. Bu çalışmada, Alzheimer hastalığının in vitro bir modelini oluşturarak melatoninin nöroblastom hücrelerinde mitokondriye bağımlı TRPA1 iyon kanalları üzerindeki etkisini araştırdık. Yöntem: Bir AH modeli oluşturmak için SH-SY5Y (insan nöroblastom hücre dizisi) hücrelerine okadaik asit uygulandı. Hücresel farklılaşma sonrası yedi ana grup (Grup 1 (Kontrol), Grup 2 (Mel+AH), Grup 3 (Mel+AH+AP18), Grup 4 (AH), Grup 5 (AH+AP18), Grup 6 (AH+Mel) ve Grup 7 (AH+Mel+AP18) oluşturuldu ve melatoninin nöroblastom hücrelerinde kalsiyuma bağımlı TRPA1 kanalları üzerindeki etkisi incelenerek in vitro Alzheimer hastalığı belirlendi. Bulgular: Kontrol grubuna göre melatonin+AH, AH ve AH+melatonin gruplarında Ca2+ konsantrasyonu daha yüksekti (p<0,001). Ancak Mel+AH+AP18, AH+Mel+AP18 ve kontrol arasında istatistiksel olarak anlamlı bir fark yoktu. Melatonin+AH ve AH+melatonin gruplarında Ca2+ düzeylerinin AH grubuna göre daha düşük olduğunu belirledik (p<0,001 ve p<0,05). Ayrıca sitozolik Ca 2+ konsantrasyonları melatonin+AH grubunda AH+melatonin grubuna göre daha düşük bulundu (p<0,05). Apoptoz ve oksidatif stres düzeylerini değerlendirirken, melatonin+AH, AH ve AH+melatonin gruplarında apoptoz ve hücre içi ROS değerlerinin kontrol grubuna göre daha yüksek olduğunu bulduk (p<0,001). Bu doğrultuda melatonin+AH , AH ve AH+melatonin gruplarında mitokondriyal depolarizasyon ve kaspaz 3 ve kaspaz 9 düzeyleri kontrol grubuna göre daha yüksekti (p<0,001). Ayrıca mitokondriyal depolarizasyon, kaspaz 3 ve kaspaz 9 değerleri AH grubunda melatonin+AH ve AH+melatonin gruplarına göre daha yüksek (p<0,001), mitokondriyal depolarizasyon ve kaspaz 3 düzeyleri melatonin+AH grubunda AH+melatonin grubundan daha düşüktü (p<0,001). Ancak aynı gruplarda kaspaz 9 sonuçlarında istatistiksel olarak anlamlı bir fark yoktu. Ayrıca kaspaz 9 değerleri melatonin+AH grubu, AH grubu ve AH+melatonin gruplarında sırasıyla melatonin+AH+AP18, AH+AP18 ve AH+melatonin+AP18 gruplarına göre daha düşüktü (p<0,001 ve p<0,05). Sonuç: Sonuçlarımız melatoninin, TRPA1 kanalları aracılığıyla sitozolik Ca2+ konsantrasyonunu, apoptozu ve hücre içi ROS’u azaltarak Alzheimer hastalığının tedavisinde ve profilaksisinde etkili bir seçenek olabileceğini düşündürmektedir.
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    Antalya’da Sağlık Turizmi Yetki Belgesi Olan Kurumlarda Dijital Pazarlamanın Etkisi
    (HTA Department of Turkish MoH, 2024) İlhan, Candan Fırtına; Övey, İshak Suat
    Sağlık turizmi, turizm alanında katma değeri en yüksek türlerden biridir ve gün geçtikçe artan bir ilgi görmektedir. İnternet teknolojilerinin yaygınlaşması, sağlık turistlerinin anında güncel tedavi hizmetleri hakkında bilgi sahibi olmalarını sağlamıştır. Dijital pazarlama hizmetleri sağlık turizmi yetki belgesine sahip kurumlar için önemli bir tanıtım ve markalaşma aracı olmuştur. Bu çalışma dijital pazarlama alanında sağlık turizmi işletmelerine yönelik bir incelemedir. Çalışma Antalya ilinde bulunan, sağlık turizmi yetki belgesi olan 10 Özel Ağız ve Diş Sağlığı Polikliniğini kapsamaktadır. Seçilen sağlık işletmelerinin web sayfaları ve sosyal medya hesapları (Facebook, YouTube, Instagram) üzerinden içerik analizi yapılarak, Dijital pazarlamanın etkisi değerlendirilmiştir. Araştırmada, literatür taraması ve içerik analizi yöntemi kullanılmıştır. Yapılan araştırma kapsamında dijital pazarlama araçlarının, sağlık tesisleri üzerinde etkili olduğunu göstermektedir. Sosyal medya araçlarını aktif kullanan sağlık tesislerinin, hastaların geri bildirimleri, hasta memnuniyet yorumları, videoları, güncel içerik üretimi gibi alanlardaki paylaşımları da dijital pazarlama araçlarının etkin kullanımının önemini göstermektedir.
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    Apoptosis Induction Through Increased TRPV1 Activation by Synergic Effect of Melatonin and Doxorubicin in Human Osteosarcoma and Chondrosarcoma Cell Lines
    (2023) Kocak, Ahmet; Gülcü, Anıl; Övey, İshak Suat
    Aim: We aimed to reveal the role of doxorubicin (Dox), melatonin (Mel) and transient receptor potential Vanilloid 1 (TRPV1) channels in bone and cartilage cancer cells during the treatment process. Human Bone Osteosarcoma (Saos-2/An1) and Human Chondrosarcoma (Hs 819.T) cell lines were used to prepare in-vitro experiment models. Methods: Both cell lines were cultured at 37°C. We have separated each cell line into five groups as follows: Controls, Dox, Dox+Capsazepine (Cpz), Dox+Melatonin (Mel), and combined Dox+Mel+Cpz given group. Capsaicin and capsazepine were added to cell culture mediums to activate or inactivate the TRPV1 channels, respectively. Cytosolic calcium, apoptosis, intracellular reactive oxygen, mitochondrial depolarization, caspase-3 and caspase-9 levels were measured. Results: Increased apoptotic activity was detected in doxorubicin given cell lines (Group II) when compared with the controls (p?0.001). There was also a significantly higher apoptotic level in Dox+Mel group (Group IV), when compared with only Dox given group (p?0.001). TRPV1 inhibition applied groups (Group III and V) have had lower apoptotic levels than other drug administered groups (p?0.001). Conclusion: This study has indicated that apoptotic effects of Dox and Mel on both osteosarcoma and chondrosarcoma were strictly associated to TRPV1 channels, and that TRPV1 channels played an important role in whole mitochondria dependent pathways of apoptosis, which in turn may lead to increased intracellular Ca+2 levels and mitochondrial depolarization.
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    Apoptotic efficiency of capecitabine and 5-fluorouracil on human cancer cells through TRPV1 channels
    (Natl Inst Science Communication-Niscair, 2020) Övey, İshak Suat; Güler, Yılmaz
    The expression of transient receptor potential protein channels increases intensively colon and breast cancer cells. We aimed to reveal the role of 5-fluorouracil (5FU) and capecitabine along with Transient Receptor Potential Vanilloid 1 (TRPV1) channels in breast and colon cancer cells. Breast (MCF-7) and colon (Caco-2) cells were cultured and the study was planned as 7 main groups. Cells in the group were incubated with 5FU and capecitabine for 24 h and then incubated with TRPV1 channel antagonist capsazepine and stimulator capsaicin. The effects of medicines were investigated on molecular pathways of apoptosis. It was concluded that the administration of TRPV1 channel stimulator capsaicin in both cancer cells significantly increased the degree of intracellular Ca2+ levels and apoptosis levels compared to the control group whereas, the use of TRPV1 channel inhibitor capsazepine, significantly decreased the degree of apoptosis levels. The apoptotic effects of 5FU and capecitabine on both colon and breast cancer cells are directly related to TRPV1 channels and TRPV1 channels play an important role in the apoptosis. The apoptotic cell lines activity of capecitabine was higher in breast cancer cells, while that of 5FU was more pronounced in colon cancer cells.
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    Effect of astaxanthin in imatinib mesylate-induced cardiotoxicity
    (Alanya Alaaddin Keykubat Üniversitesi, 2020) Övey, İshak Suat; Öncel, Can Ramazan
    Aim: Imatinib mesylate is a tyrosine kinase inhibitor and is approved as a standard first-line therapy of chronic myeloid leukemia. Oxidative stress, as well as intracellular calcium overload and mitochondrial dysfunction, play an important role in chemotherapy-induced cardiotoxicity. The underlying pathophysiological mechanism associated with imatinib-induced cardiotoxicity is not well understood. In the present study, we investigated alterations in calcium influx, oxidative stress and apoptosis through transient receptor potential melastatin 2 (TRPM2) channels. Also, we aimed to investigate if there is a modulator role of astaxanthin in cardiomyocytes during imatinib mesylate-induced cardiotoxicity. Materials and methods: The cells were divided into seven main control groups: imatinib, imatinib+antranilic acid, imatinib+astaxanthin, imatinib+antranilic acid+astaxanthin, astaxanthin and astaxanthin+antranilic acid groups. Cells in the groups were stimulated with cumene hydroperoxide and inhibited with antranilic acid in related experiments for activation and inactivation of TRPM2 channels, respectively. We measured cytosolic calcium, intracellular reactive oxygene, mitochondrial depolarization, caspase 3 and caspase 9 levels.Results: The apoptosis values were significantly lower in the astaxanthin and the imatinib+astaxanthin group than in the imatinib group of cardiomyocytes (p&lt; 0.001). The cell viability values were significantly higher in the imatinib+astaxanthin+antranilic acid (p&lt;0.001) and the imatinib+astaxanthin (p&lt;0.05) groups, than in the imatinib group.Conclusions: As a result, we found that TRPM2 channels were found in cardiomyocyte cells and they were activated by reactive oxygen species. Also, we showed that overactivated TRPM2 channels are associated with increased cytosolic free calcium, oxidative stress and apoptotic cell injury in imatinib mesylate-induced cardiotoxicity, whereas astaxanthin could have a modulator role in this instance.
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    Effects of homocysteine and memantine on oxidative stress related TRP cation channels in in-vitro model of alzheimer's disease
    (Wiley, 2018) Övey, İshak Suat; Nazıroğlu, Mustafa
    [No abstract available]
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    Effects of homocysteine and memantine on oxidative stress related TRP cation channels inin-vitromodel of Alzheimer's disease
    (Taylor & Francis Ltd, 2020) Övey, İshak Suat; Nazıroğlu, Mustafa
    Memantine (MEM) has been used to treat patients with Alzheimer' disease though inhibition of reactive oxygen species (ROS), Ca(2+)entry and glutamate receptor. The Ca(2+)permeable TRPA1, TRPM2 and TRPV1 channels are activated in the hippocampus by ROS, and antioxidant MEM as a potent TRPA1, TRPM2 and TRPV1 channel antagonist may reduce A beta-induced oxidative stress and apoptosis in the neurons. In the current study, we investigated the neuroprotective properties of MEM in A beta-induced hippocampal neuron cultures. Freshly isolated hippocampal neurons of mice were divided into eight groups as control, A beta, Hcy, MEM, A beta + Hcy, A beta + Hcy + MEM, A beta + MEM and Hcy + MEM. The neurons were exposed to incubated with A beta (20 mu M for 24 h), Hcy (250 mu M for 30 min) and MEM (10 mu M for 24 h). TRPA1, TRPM2 and TRPV1 of the eight groups were further stimulated by cinnamaldehyde, cumene hydyroperoxide and capsaicin, respectively although they were further inhibited by AP-18, N-(p-Amylcinnamoyl) anthranilic acid (ACA) and capsazepine (CPZ). The [Ca2+] concentration, apoptosis, caspase 3, caspase 9 activations, mitochondrial membrane depolarization and intracellular ROS production values in the neurons were higher in A beta and Hcy groups than in control although they were lower in the MEM group than in A beta and Hcy groups. The values were further decreased by MEM + AP-18, MEM + CPZ and MEM + ACA treatments as compared to MEM only. A beta and Hcy-induced decrease of cell viability level was increased by MEM treatment although A beta and Hcy-induced increase of caspase 3, caspase 9, PARP1, TRPA1, TRPM2 and TRPV1 expression levels were decreased by MEM treatments. In conclusion, TRPA1, TRPM2 and TRPV1 channels are involved in A beta and Hcy-induced neuronal death, and modulation of the activity of these channels by MEM treatment may account for their neuroprotective activity against apoptosis, excessive ROS production, and Ca(2+)entry.
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    Ginkgo Biloba Özütünün in Vitro Alzheimer Hastalığı Modelinde TRPV1 Kanalları Aracılığıyla Koruyucu ve Terapötik Rolü
    (2023) Özşimşek, Ahmet; Övey, İshak Suat; Karacay, Ertan; Yuluğ, Burak
    Amaç: Ginkgo biloba’nın (GB) nöroblastom hücrelerinde mitokondriye bağımlı TRPV1 iyon kanalları üzerindeki etkisi Alzheimer hastalığı (AH) modeli oluşturularak araştırıldı. Yöntem: Bir AH modeli oluşturmak için SH-SY5Y hücrelerine okadaik asit uygulandı. Hücresel farklılaşmadan sonra yedi ana grupla organize edilen çalışma, GB’nin nöroblastom hücrelerinde AH’de kalsiyuma bağlı TRPV1 kanallarına etkisinin incelendiği in vitro çalışmadır. Bulgular: Kontrol grubu ile karşılaştırıldığında GB+AH, AH ve AH+GB gruplarında daha yüksek Ca 2+ konsantrasyonu saptandı (p<0,001). Ca 2+ düzeyi GB+AH ve AH+GB gruplarında AH grubuna göre daha düşüktü (p<0,001). Ayrıca GB+AH’de sitozolik Ca 2+ konsantrasyonu AH+GB grubuna göre daha düşüktü (p<0,05), apoptoz ve hücre içi reaktif oksijen türleri (ROS) değerleri GB+AH, AH ve AH+GB’de control grubuna göre daha yüksekti (p<0,001). Apoptoz ve hücre içi ROS değerleri AH grubunda GB+AH ve AH+GB grubuna göre daha yüksekti (p<0,001) ve AH+GB grubunda apoptoz düzeyi GB+AH grubuna göre daha yüksekti (p<0,001) ve mitokondriyal depolarizasyon, kaspaz 3 ve kaspaz 9 düzeyleri GB+AH, AH ve AH+GB gruplarında kontrol grubuna göre daha yüksekti (p<0,001). Ayrıca GB+AH+kapsazepin grubu, AH+kapsazepin grubu ve AH+GB+kapsazepin ile karşılaştırıldığında GB+AH grubu, AH grubu ve AH+GB gruplarında değerler daha düşüktü (p<0,001). Sonuç: Bu sonuçlar bize GB’nin TRPV1 kanalı üzerinden Alzheimer hastalığında tedavi edici etkisinin yanında koruyucu etkisinin olduğunu göstermektedir.
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    LLLT enhance cyclophosphamide induced TRPM2 channel activation in human colon cancer cells
    (Comenius Univ, 2020) Güler, Yılmaz; Övey, İshak Suat
    AIM: Transient receptor potential (TRP) channels expression is enhanced significantly in colon cancer cells and Low Lever Laser Treatment (LLLT), is known to have effects and is used clinically in the treatment ofmany diseases, including colon cancer. We aimed to reveal the effects of (LLLT) on apoptosis of colon cancer and on the efficacy of cyclophosphamide via Transient receptor potential melastatin 2 (TRPM2) channels. METHOD: Human colon cancer cells (Caco-2) were cultured and cells were divided into seven main groups. Cells were incubated with cyclophosphamide, TRPM2 channel inhibitor, stimulator and low level laser exposure separately and together. The effects of cyclophosphamide and low level laser were investigated on apoptosis. RESULTS: It was found that the levels of apoptosis in cyclophosphamide group were significantly increased in cancer cells compared to the control group. TRPM2 channel stimulator administration resulted in significantly increased apoptosis levels compared to the control group, in cyclophosphamide + low level laser group the apoptosis level was significantly increased compared to the cyclophosphamide-only group. CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig. 5, Ref. 26).
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    Low level laser application reduces the effect of 5 fluorouracil/leucovorin combination on human breast cancer cells
    (2020) Güler, Yılmaz; Övey, İshak Suat; Samur, Dilara Nemutlu; Karabulut, Bayhan
    Aim : 5-fluorouracil has been widely used in breast cancer treatment. Low level laser therapy (LLLT) has been shown to modulate biological processes and used in cancer treatment. It has been reported that apoptosis is induced by stimulation of transient receptor potential protein channels in numerous cancer cells, including breast cancer. We aimed to reveal the effects of 5-fluorouracil / Leucovorin (5-FU/LV) and . low level laser on apoptosis via transient receptor protein ancyrin 1 (TRPA1) channels. Material and Methods: Breast cancer cells (MCF-7) were cultured and cells were divided into seven main groups. Cells were incubated with 5-FU/LV and LLLT exposure separately and together performed on MCF-7 cell cultures. Cell cultures incubated with TRPV1 channel antagonist capsazepin and stimulator capsaicin. The effects of 5-FU and LLLT were investigated on all molecular pathways of apoptosis. Results: It was found that the levels of apoptosis in 5-FU/LV group were significantly increased in cancer cells compared to control group .TRPA1 channel stimulator administration resulted in significantly increased apoptosis levels compared to the control group, in 5-FU/LV + low level laser group the apoptosis level significantly reduced compared to 5-FU/LV-only group. (p<0.001) Conclusion: It has been shown that 5-FU/LV significantly increases apoptosis in breast cancer cells, however low level laser administration decreases apoptosis and suppressed apopitotic effect of 5-FU/LV significantly on breast cancer cells.
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    LOW LEVEL LASER THERAPY REDUCES ANTICANCER POTENTIAL OF COLLOIDAL SILVER THROUGH TRPV1 CHANNELS SHORT TITLE: LLLT REDUCES ANTICANCER POTENTIAL OF COLLOIDAL SILVER
    (Interciencia Association, 2023) Övey, İshak Suat; Güler, Yilmaz; Celik, O.
    Background: Recently there are studies which particularly investigated efficiency of silver on neoplastic diseases. and many other diseases. Low level laser therapy (LLLT) has been shown to modulate biological processes and there are many studies that investigate the effect of LLLT, which is used in the treatment of cancers currently. Methods: Breast (MCF7) and colon (Caco-2) cells were cultured and cells were divided into seven main groups. Cells were incubated with colloidal silver for 24 hrs. Colloidal silver and LLLT exposure separately and together performed on MCF7 and Caco-2 cell cultures. The effects of colloidal silver and LLLT were invastigated on mitochondrial pathways of apoptosis. Results: It was found that the levels of apoptosis in colloidal silver group were significantly increased in both cancer cells compared to control group. In both cancer cells, transient receptor protein vanilloid 1 (TRPV1) channel stimulator Cpcn administration resulted in significantly increased apoptosis levels compared to the control group, in colloidal silver + 650nm (LLLT) group the apopitosis level significantly reduced compared to colloidal silver-only group. Conclusions: It has been shown that colloidal silver significantly increases apoptosis in breast and colon cancer cells, however LLLT administration decreases apoptosis in both wavelength and suppressed apoptotic effect of colloidal silver significantly on these cells. © 2023 Interciencia Association. All rights reserved.
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    Protective effects of N-acetyl cysteine against paclitaxel-induced cardiotoxicity through modulation of transient receptor potential melastatin 2 channels
    (Gazi Univ, Fac Med, 2019) Öncel, Can Ramazan; Övey, İshak Suat
    Aim : In our study, we investigated the paclitaxel induced cardiotoxicity and alterations in Ca2+ influx, oxidative stress and apoptosis through transient receptor potential melastatin 2 (TRPM2) channels and modulator role of N-acetyl cysteine (NAC) in cardiomyocytes. Material and Methods : All cells were cultured at 37 degrees C. The cells were divided into seven main groups. Cells in the paclitaxel group were incubated with 2.5 mu M Paclitaxel for 12 hours and cells in the NAC+Paclitaxel group were incubated with 2.5 mu M Paclitaxel for 12 hours and then incubated with 10 mu M NAC for 24 hours. Intracellular free calcium concentration, reactive oxygen species (ROS) production measurements and cell viability analyses were done according to the study protocol. Results : Cytosolic calcium levels, apoptosis levels, intracellular ROS production levels were lower in paclitaxel+NAC group than in the paclitaxel group of cardiomyocytes. Also values were markedly lower in the paclitaxel+NAC+antranilic acid group when compared to the paclitaxel+ NAC group. Conclusion : We found that TRPM2 channels are overactivated during paclitaxel induced cardiotoxicity and NAC could show a cardioprotective effect through TRPM2 channel modulation.
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    Selenium enhances the TRPM2 mediated effect of paclitaxel on human breast cancer cells
    (2020) Güler, Yılmaz; Övey, İshak Suat
    Abstract Aim: Paclitaxel is widely used in adjuvant treatment of early breast cancer and second-line treatment of metastatic breast cancer. It has been reported that transient receptor potential melastatin-2 (TRPM2) channels are expressed intensively in breast cancer and has significant effects on oxidative stress. Selenium is an essential element and has effects on reproduction, toxicity, antiaging and DNA reproduction. In this study, we aimed to reveal the role of selenium and TRPM2 channels on apoptotic effects of paclitaxel in breast cancer cells. Material and Methods: Breast cancer cells (MCF-7) were cultured and cells were divided into seven main groups. Cells were incubated with paclitaxel and selenium separately and together administrated on breast cancer cell cultures. Cell cultures incubated with TRPM2 channel antagonist anthranilic acid and stimulator cumene-hydroperoxyde. The effects of paclitaxel and selenium were invastigated on molecular pathways of apoptosis. Results: It was found that the levels of apoptosis in paclitaxel group were significantly increased in cancer cells compared to control group (p<0,001).TRPM2 channel stimulator cumene-hydroperoxyde administration resulted in significantly increased apoptosis levels compared to the control group (p<0.001) and it was found that in pacliatxel + selenium group the apopitosis level significantly increased compared to paclitaxel-only group (p<0.001). Conclusion: As a result of our study, it has been shown that paclitaxel significantly increases apoptosis in breast cancer cells, and this effect directly related the TRPM2 channels. It was found that the application of selenium in cell culture medium in non-toxic doses increased the TRPM2 mediated apoptotic activity of paclitaxel.
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    Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells
    (2020) Özkal, Birol; Övey, İshak Suat
    Purpose Neuroblastoma is a malignant solid tumor that originates from the sympathetic nervous system in early childhood. Temozolomide is used for treatment in high-risk groups with low treatment response of neuroblastomas. TRPA1 channels in neuroblastoma cells are calcium permeable channels that can be activated by reactive oxygen species (ROT). In this study, we aimed to evaluate the level of activity of temozolomide and selenium in neuroblastoma cells via TRPA1 channels. Method Seven main groups were formed using SH-SY5Y neuroblastoma cells. The control was divided into temozolomide (TMZ) (100 ?M, 24 h), TMZ+SEL+AP18, SEL (sodium selenite, 100 ?M, 24 h), and SEL+AP18 groups. Intergroup calcium signaling, intracellular reactive oxygen species, caspase-3 and caspase-9, and mitochondrial depolarization analyses were performed by channel activation with TRPA1 agonist cinnamaldehyde in all groups. Results Cytosolic calcium concentration, apoptosis, caspase-3 and caspase-9 activation, mitochondrial membrane depolarization, and ROT levels were higher in TMZ (p < 0.001), TMZ+SEL (p < 0.001), and SEL (p < 0.05) groups than the control group. TRPA1 was lower in TTMZ+AP18, TMZ+SEL+AP18, and SEL+AP18 groups with channel blockers than respectively TMZ, TMZ+SEL, and SEL groups without channel blockers (p < 0.05). Conclusion The use of selenium with temozolomide increased the apoptotic efficacy of temozolomide via TRPA1 channels on tumor cells
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    Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells
    (Springer, 2020) Özkal, Birol; Övey, İshak Suat
    Purpose Neuroblastoma is a malignant solid tumor that originates from the sympathetic nervous system in early childhood. Temozolomide is used for treatment in high-risk groups with low treatment response of neuroblastomas. TRPA1 channels in neuroblastoma cells are calcium permeable channels that can be activated by reactive oxygen species (ROT). In this study, we aimed to evaluate the level of activity of temozolomide and selenium in neuroblastoma cells via TRPA1 channels. Method Seven main groups were formed using SH-SY5Y neuroblastoma cells. The control was divided into temozolomide (TMZ) (100 mu M, 24 h), TMZ+SEL+AP18, SEL (sodium selenite, 100 mu M, 24 h), and SEL+AP18 groups. Intergroup calcium signaling, intracellular reactive oxygen species, caspase-3 and caspase-9, and mitochondrial depolarization analyses were performed by channel activation with TRPA1 agonist cinnamaldehyde in all groups. Results Cytosolic calcium concentration, apoptosis, caspase-3 and caspase-9 activation, mitochondrial membrane depolarization, and ROT levels were higher in TMZ (p < 0.001), TMZ+SEL (p < 0.001), and SEL (p < 0.05) groups than the control group. TRPA1 was lower in TTMZ+AP18, TMZ+SEL+AP18, and SEL+AP18 groups with channel blockers than respectively TMZ, TMZ+SEL, and SEL groups without channel blockers (p < 0.05). Conclusion The use of selenium with temozolomide increased the apoptotic efficacy of temozolomide via TRPA1 channels on tumor cells.
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    Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells (vol 21, pg 541, 2020)
    (Springer, 2020) Özkal, Birol; Övey, İshak Suat
    [No abstract available]
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    Synergic and comparative effect of 5-fluorouracil and leucoverin on breast and colon cancer cells through TRPM2 channels
    (Comenius Univ, 2018) Güler, Yılmaz; Övey, İshak Suat
    OBJECTIVES: We aimed to reveal the role of 5-fluorouracil (5-FU) and Leucovorin (LV) along with transient receptor potential protein melastatin 2 (TRPM2) channels in breast and colon cancer cells during the treatment process. BACKGROUND: 5-FU and LV are widely used in breast and colon cancers for chemotherapy. It has been reported that the expression of TRPM2 channels increased intensively in cancer cells. METHODS: Breast (MCF7) and colon (Caco-2) cells were cultured and divided into seven main groups. The cells in the group were incubated with 5-FU and LV for 24 hrs and then incubated with Antranilic acid. The effects of medicines were investigated on all molecular pathways of apoptosis. RESULTS: It was found that 5FU and LCV, administered separately and together on breast cancer cell culture and colon cancer cell culture increased the intracellular calcium levels by stimulation of TRPM2 channels in both cancer cells. CONCLUSION: As the result of our study, it has been shown that apoptotic effects of 5FU and LV on both colon and breast cancer cells were directly related to TRPM2 channels and that TRPM2 channels played an important role in the whole molecular pathway of apoptosis leading to increased intracellular Ca2+ (Ca2+) levels and increased mitochondrial depolarisation (Fig. 6, Ref. 43). Text in PDF www.elis.sk.
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    Öğe
    The effect of melatonin on digoxin-induced cardiac damage in cardiomyocytes
    (Comenius Univ, 2019) Övey, İshak Suat; Öncel, Can Ramazan
    OBJECTIVES: Digoxin is a cardiac glycoside which is widely used in cardiovascular medicine. Oxidative stress, as well as intracellular Ca2+ overload, plays an important role in digoxin toxicity. Transient receptor potential vanilloid 1 (TRPV1) channels are found in cardiomyocyte cells and they are activated by reactive oxygen species. We investigated the effects of digoxin toxicity and alterations in Ca2+ influx, oxidative stress and apoptosis through TRPV1 channels and modulator role of melatonin in cardiomyocytes. METHODS: The cells were divided into seven main groups as control, digoxin, digoxin+capsazepine, digoxin+melatonin, digoxin+capsazepine+melatonin, melatonin and melatonin+capsazepine groups. Cells in the groups were stimulated with capsaicin and inhibited with capsazepine in related experiments for activation and inactivation of TRPV1 channels, respectively. We measured cytosolic calcium, intracellular reactive oxygen, mitochondrial depolarization, caspase 9 and caspase 3 levels. RESULTS: The apoptosis values were significantly lower in the melatonin and digoxin+ melatonin groups than in the digoxin group of cardiomyocytes (p < 0.001). The cell viability values were higher in the digoxin+ capsazepine (p < 0.001), digoxin+melatonin (p < 0.001) and digoxin+melatonin+capsazepine (p < 0.001) groups than in the digoxin group. CONCLUSION: TRPV1 channels are overactivated during digoxin toxicity and melatonin could show a cardioprotective effect through TRPV1 channel modulation (Fig. 5, Ref. 56).