Person: GÜNAYDIN AKYILDIZ, AYŞENUR
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Publication Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity(2019-09-01T00:00:00Z) Boran, Tuğçe; Günaydın, Ayşenur; Jannuzzı, Ayşe Tarbın; Özçağlı, Eren; Alpertunga, Büket; GÜNAYDIN AKYILDIZ, AYŞENURCelastrol is a natural bioactive compound extracted from the medicinal plant Tripterygium wilfordii Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effective therapeutically, it can cause nephrotoxicity leading to dose reduction or discontinuation of treatment. This study aims to clarify the therapeutic potential of celastrol in cisplatin-induced nephrotoxicity. The possible protective effects of celastrol pretreatment against cisplatin-induced oxidative stress and genotoxicity were investigated. A rat kidney epithelial cell line NRK-52E was pretreated with the desired concentrations of celastrol (200 nM, 100 nM, and 50 nM) for 24 h. The cells were treated with 50 mu M cisplatin for a further 24 h to see whether cisplatin caused the same or less toxicity compared to the vehicle control group. Alkaline comet assay was performed for genotoxicity assessment. Genotoxicity evaluation revealed that celastrol caused a statistically significant reduction in DNA damage. Oxidative stress parameters were evaluated by measuring the glutathione (GSH) and protein carbonyl (PC) levels and also by measuring the enzyme activities of glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) enzymes. Celastrol pretreatment increased the GSH content of the cells and ameliorated the protein carbonylation level. Likewise, celastrol pretreatment improved the GR and CAT activities. However, no significant difference was observed in GPx and SOD activities. In the light of these findings, celastrol treatment could be a therapeutic option to reduce cisplatin-induced nephrotoxicity. Further studies are needed for the clarification of its therapeutic potential.Publication An evaluation of a hepatotoxicity risk induced by the microplastic polymethyl methacrylate (PMMA) using HepG2/THP-1 co-culture model(2024-04-01) Boran T.; Zengin Ö. S.; Şeker Z.; Günaydın Akyıldız A.; Kara M.; Öztaş E.; Özhan G.; ŞEKER, ZEHRA; GÜNAYDIN AKYILDIZ, AYŞENURPublication Ivermectin Induces Oxidative Stress and DNA Damage in Breast Cancer Cells(2023-01-01) Güler E. M.; Günaydın Akyıldız A.; GÜNAYDIN AKYILDIZ, AYŞENURObjective: Breast cancer (BC) remains to be one of the most diagnosed cancer types among women around the world. Drug repurposing is suggested to be a convenient alternative for drug development in cancer treatment. Ivermectin, the antiparasitic agent produced by the bacterium Streptomyces avermitilis, is currently being examined thoroughly in oncology and has begun to be seen as a potential drug candidate for BC therapy. However, studies are limited, and the exact anti-tumorigenic mechanism is not yet clarified in breast cancer. Methods: For elucidating the molecular mechanisms of Ivermectin’s potential anticancer effects, we have examined its in vitro effects on BC cells in terms of cell viability, intracellular ROS levels, glutathione levels, mitochondrial membrane potential, apoptosis, and DNA damage. Results: Ivermectin induces apoptosis via oxidative stress and DNA damage in BC cells. Conclusion: The in vitro mechanistic studies of promising anticancer agents for repurposing are essential guides for drug developers. For this purpose, ivermectin should be further studied as a drug candidate for its potential in the treatment of breast cancer.Publication Design, synthesis, cytotoxicity, and PARP-1 inhibitor activity of novel hydrazide-hydrazone compound containing 1,2,4-triazole ring(2022-03-14T00:00:00Z) Coşar, Ebru Didem; Günaydın Akyıldız, Ayşenur; Ece, Abdulilah; Güzeldemirci, Nuray; COŞAR, EBRU DİDEM; GÜNAYDIN AKYILDIZ, AYŞENURPublication Favipiravir Induces Oxidative Stress and Genotoxicity in Cardiac and Skin Cells.(2022-09-21T00:00:00Z) Gunaydin-Akyildiz, AYŞENUR; Aksoy, Nergis; Boran, Tugce; Ilhan, Emine Nihan; Ozhan, Gul; GÜNAYDIN AKYILDIZ, AYŞENURFavipiravir (T-705), used against influenza viruses, is approved for emergency use in many countries for the treatment of COVID-19. The frequent adverse effects of favipiravir are related with the gastrointestinal system, however, studies suggest a positive association of favipiravir on QTc prolongation, which can cause cardiotoxicity. Also, there are reports of skin reactions such as angioedema due to favipiravir. Despite the several adverse effects, studies examining the drug's effects at the molecular level are insufficient, e.g., the genotoxic and oxidative stress-inducing effects of favipiravir, which are among the primary mechanisms of drug-induced toxicity. The cytotoxicity of favipiravir was analyzed with the measurement of the ATP content in H9c2 cardiomyoblasts and CCD-1079Sk skin fibroblasts. The ATP level decreased starting from 200 µM. The inhibitory effect on the mitochondrial electron transport chain enzymes complex I and complex V was also evaluated where favipiravir showed significant enzyme inhibitory effects in the highest concentration studied. A molecular docking study evaluating the interaction between favipiravir-RTP and mitochondrial DNA polymerase (POLG1) was done. The relationship of favipiravir with oxidative stress was examined by measuring glutathione (GSH) and protein carbonyl levels which were observed higher after drug treatment compared to the control group. The genotoxicity study was done using the Comet assay and increase in DNA tail has been detected. Furthermore, 8-OHdG levels were measured higher in favipiravir treated cells indicating oxidative DNA damage. Favipiravir induced oxidative stress leading to DNA damage in cardiomyoblast cells and fibroblastic skin cells. Oxidative stress and DNA damage might eventually lead to organ-specific damage such as cardiotoxicity and dermal toxicity. Considering the increased use of favipiravir in recent years, and that oxidative stress and genotoxicity are two important indicators of drug-induced toxicity, the obtained results are worth attention.Publication Extended regorafenib treatment can be linked with mitochondrial damage leading to cardiotoxicity.(2020-11-06T00:00:00Z) Boran, T; Akyildiz, AYŞENUR; Jannuzzi, AT; Alpertunga, B; GÜNAYDIN AKYILDIZ, AYŞENURPublication In Vitro Investigation of the Antineoplastic Agent Lenvatinib Induced Cardiotoxicity in Terms of Mitochondrial Toxicity(2019-03-14) GÜNAYDIN, AYŞENUR; Boran, Tuğçe; Jannuzzi, Ayşe Tarbın; Alpertunga, Buket; GÜNAYDIN AKYILDIZ, AYŞENURPublication Karvon, Karvakrol ve Kamforun Aspergillus flavus ile Biyotransformasyonuyla Olusan Metabolitlerin Analitik Yöntemlerle Tayini ve Sitotoksik Aktivitelerinin Belirlenmesi(2020-09-20T00:00:00Z) Gazioğlu, Işıl; Zengin, Özge Sultan; Günaydın Akyıldız, Ayşenur; GÜNAYDIN AKYILDIZ, AYŞENURPublication Emodin and aloe-emodin, two potential molecules in regulating cell migration of skin cells through the MAP kinase pathway and affecting Caenorhabditis elegans thermotolerance(2023-12-01) GÜNAYDIN AKYILDIZ, AYŞENUR; Yanikoglu R. S.; Gulec M.; ALİM TORAMAN, GÜLBAHAR ÖZGE; Kuran E. D.; Atasoy S.; Olgun A.; Topcu G.; TOPÇU, GÜLAÇTI; ATASOY, SEZEN; GÜNAYDIN AKYILDIZ, AYŞENUR; ALİM TORAMAN, GÜLBAHAR ÖZGE; YANIKOĞLU, RABİA SAREBackground: Emodin and aloe-emodin are two anthraquinones having positive effects in wound healing. However, their mechanism of action of wound healing is not fully understood. The MAP kinase family, which plays an active role in wound healing, is a well-characterized large family of serine/threonine kinases and regulates processes such as proliferation, oncogenesis, differentiation, and inflammation in the cell. The aim of this study is to comparatively elucidate the mechanisms of action of emodin and aloe-emodin, which are potential agents in wound healing. Methods: The mechanism of the effects of emodin and aloe-emodin on cell viability and cell migration was examined using the human skin fibroblast (CCD-1079Sk) cell line. The gene expression levels of the MAP kinases (JNK, P38, ERK) in the skin fibroblast cells along with a molecular docking study analyzing their interaction potential were evaluated. Furthermore, the molecules’ effects on the lifespan of Caenorhabditis elegans were studied. Results: Emodin and aloe-emodin inhibited the ATP content of the cells in a concentration dependent manner and accelerated cell migration at the lower concentrations while inhibiting cell migration in the higher concentration treatment groups. The expressions of JNK and P38 were upregulated at the low concentrations and downregulated at the higher concentrations. The molecular docking studies of the molecules gave high docking scores indicating their interaction potential with JNK and P38. C. elegans lifespan under heat stress was observed longer after 75 µM emodin and was significantly reduced after 150 µM aloe-emodin treatment. Conclusion: Aloe-emodin was found to be more potent on cell viability, cell migration, gene expression levels of the MAP kinases in healthy fibroblastic skin cells, and on the lifespan of C. elegans. This study reveals the functional effects and the biological factors that interact in the wound healing process of emodin and aloe-emodin, and give a possible treatment alternative to shorten the duration of wound care.Publication Cardiotoxicity Induced by Tyrosine Kinase Inhibitors(2019-10-16) Günaydın, Ayşenur; Boran, Tuğçe; Jannuzzı, Ayşe Tarbın; Alpertunga, Büket; GÜNAYDIN AKYILDIZ, AYŞENUR
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