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    Alternations in interleukin-1? and nuclear factor kappa beta activity (NF-kB) in rat liver due to the co-exposure of Cadmium and Arsenic: Protective role of curcumin
    (Elsevier, 2023) Cengiz, Mustafa; Gur, Bahri; Sezer, Canan Vejselova; Cengiz, Betuel Peker; Gur, Fatma; Bayrakdar, Alpaslan; Ayhanci, Adnan
    Cadmium chloride (Cd) and sodium arsenite (As) are two prominent examples of non-biodegradable substances that accumulate in ecosystems, pose a serious risk to human health and are not biodegradable. Although the toxicity caused by individual use of Cd and As is known, the toxicity of combined use (Cd+As) to mammals is poorly understood. The present study aims to investigate the hepatoprotective effect of curcumin (CUR), a naturally occurring bioactive component isolated from the root stem of Curcuma longa Linn., in preventing liver damage caused by a Cd+As mixture. A group of 30 Sprague-Dawley rats were subjected to intraperitoneal administration of Cd+As (0.44 mg/kg+5.55 mg/kg i.p.) and CUR (100 or 200 mg/kg) for a period of 14 days. The experimental results showed that the animals treated with Cd+As exhibited changes in liver biochemical parameters, inflammation and oxidative stress at the end of the experiment. Administration of CUR significantly reduced inflammation, oxidative stress and lipid peroxidation in the Cd+As plus CUR groups compared to the Cd+As group. Furthermore, histological examination of the liver tissue showed that administration of CUR had led to a significant reduction in the liver damage observed in the Cd+As group. The present study provides scientific evidence for the protective effects of CUR against lipid peroxidation, inflammation, oxidative stress and liver damage induced by Cd+As in the liver of rats. The results of our in vivo experiments were confirmed by those of our molecular modelling studies, which showed that CUR can enhance the diminished antioxidant capacity caused by Cd+As.
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    The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats
    (Elsevier Ltd, 2024) Cengiz, Mustafa; Gür, Bahri; Gür, Fatma; Şahintürk, Varol; Bayrakdar, Alpaslan; Şahin, Ilknur Kulcanay; Başkoy, Sıla Appak
    Cyclophosphamide (CP) is an alkylating anticancer drug with broad clinical application that is highly effective in the treatment of cancer and non-malignant diseases. However, the main limiting effect of CP is multi-organ toxicity due to damage to normal tissues. The aim of this study is to compare the hepatoprotective potential of selenium (Se) and boron (B) in CP-induced liver injury in experimental rats. The rats were randomly divided into six equal groups: Control (saline), 200 mg/kg CP (administered once on the fourth day of the experiment), 1.5 mg/kg Se (administered once/time daily for 6 days), 20 mg/kg B (administered once/time daily for 6 days), Se + CP and B + CP administered intraperitoneally (i.p.). Administration of CP leads to an increase in the levels of apoptotic markers (Bax, caspase-3), the apoptotic signaling pathway (Nrf2), oxidative stress indicators (TOS, OSI), lipid peroxidation markers (MPO, MDA), inflammation levels (NF-kB, TNF-?, IL-1?, IL -6), liver function markers (ALT, AST, ALP), while apoptosis markers (Bcl-2), apoptosis pathway (Keap-1), oxidative stress indicator (TAS), inflammation (IL -10) and intracellular antioxidant defense system (SOD, CAT, GPx and GSH) decreased. In addition, degeneration of hepatocytes and congestion in the central veins were observed. In contrast, in the groups administered Se and B with CP, the changes that occurred were reversed. However, it was found that Se protects the liver slightly better against CP damage than B. The protective effect of Se and B against the toxic effects of CP on the antioxidant markers SOD, CAT and GPx1 was also investigated in silico. The in silico results were consistent with the in vivo results for SOD and CAT, but not for GPx1. © 2024
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    The role of Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways in mediating the protective effect of boric acid on acrylamide-induced acute liver injury in rats
    (Pergamon-Elsevier Science Ltd, 2022) Cengiz, Mustafa; Ayhanci, Adnan; Akkemik, Ebru; Sahin, Ilknur Kulcanay; Gur, Fatma; Bayrakdar, Alpaslan; Cengiz, Betul Peker
    Introduction: This study aims to investigate whether boric acid (BA) can protect rats from acrylamide (AA)induced acute liver injury. Materials and methods: AA was used to induce acute liver injury. Thirty rats were divided into five group including Group 1 (saline), Group 2 (AA), Group 3 (20 mg/kg BA), Group 4 (10 mg/kg BA+AA) and Group 5 (20 mg/kg BA+AA). Their blood and liver were harvested to be kept for analysis. Liver function enzyme activities were performed by spectrophotometric method. Catalase (CAT), superoxide dismutase (SOD) activity, and malondialdehyde levels were determined by colorimetric method. The in-silico studies were performed using the blind docking method. Results: Administration AA to rats, biochemical parameters, liver histology, and expression levels of apoptotic markers were negatively affected. However, after the administration of BA, the altered biochemical parameters, liver histology, and expression levels of apoptotic markers were reversed. Moreover, the mechanisms of AA-induced deterioration in the levels of SOD, CAT, and Nrf2-Keap-1 and the mechanisms of the protective effect of BA against these deteriorations were explained by in silico studies. Conclusion: Thus, the present study could explain the interactions between AA and thiol-containing amino acid residues of Keap-1, the effect of BA on these interactions, and the biochemical toxicity caused by the AA. In this sense, this work is the first of its kind in the literature. Based on the biochemical, histopathological, and in silico results, it can be suggested that BA has the potential to be used as a protective agent against AA-induced liver injury.
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    The role of ceranib-2 and its nanoform on the decrease of telomerase levels in human non-small cell cancer
    (Springer, 2024) Cengiz, Mustafa; Sezer, Canan Vejselova; Gur, Bahri; Bayrakdar, Alpaslan; Izgordu, Hueseyin; Alanyali, Filiz; Ozic, Cem
    BackgroundCeranib-2, an acid ceramidase (AC) inhibitor, can inhibit cancer cell proliferation and tumor development. However, poor water solubility and low cellular bioavailability limit its efficacy in cancer treatment.Methods and resultsThis study aimed to investigate the cell death induced by ceranib-2 and its solid lipid nanoformulation (ceranib-2-SLN) produced by the hot homogenization technique and the synergistic relationship between ceramide and telomerase in vitro and in silico. Furthermore, this study proved the possible mechanism of ceranib-2-induced AC inhibition by in silico studies. The effective cytotoxic concentrations of ceranib-2, telomerase level, and changes in ceramide levels were measured by MTT colorimetric cytotoxicity assay, ELISA, and LC/MS/MS methods, respectively. TEM results showed that ceranib-2-SLN was 13-fold smaller than the size of ceranib-2. Ceranib-2 and ceranib-2-SLN had IC50 concentrations of 31.62 (+/- 2.1) and 27.69 (+/- 1.75) mu M in A549, and 48.79 (+/- 1.56) and 67.98 (+/- 2.33) in Beas-2B cells. These compounds simultaneously increased ceramide levels and decreased telomerase levels in A549 cells. Ceranib-2 increased telomerase levels while decreasing ceramide levels in Beas-2B cells. It was shown how the synergistic impact of ceranib-2-induced ceramide production and ceramide-induced telomerase level reduction on cytotoxicity in A549 cells.ConclusionsCeranib-2-SLN was discovered to be more cytotoxic on cancer cells than ceranib-2, suggesting that it could be a promising option for the development of a new anti-cancer agent.