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SÜZGÜN, PELİN

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PELİN

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2013 - 20163
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End date: 2019 × Has files: true ×

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    Anti-cancer and anti-hepatitis C virus NS5B polymerase activity of etodolac 1,2,4-triazoles
    (TAYLOR & FRANCIS LTD, 2015-09-03) SÜZGÜN, PELİN; Cikla-Suzgun, Pelin; Kaushik-Basu, Neerja; Basu, Amartya; Arora, Payal; Talele, Tanaji T.; Durmaz, Irem; Cetin-Atalay, Rengul; Kucukguzel, S. Guniz
    Arachidonic acid is an unsaturated fatty acid liberated from phospholipids of cell membranes. NSAIDs are known as targets of cyclooxygenase enzyme (COX-1, COX-2 and COX-3) in arachidonic acid metabolism. This mechanism of COX-2 in carcinogenesis causes cancer. In addition, COX-2 plays a role in the early stages of hepatocarcinogenesis. Hepatitis C virus (HCV) infection is cause of liver cirrhosis and hepatocellular carcinoma (HCC). The aim of our study was to improve effective agents against HCV. A novel series of new etodolac 1,2,4-triazoles derivatives (4a-h) have been synthesized and investigated for their activity against HCV NS5B polymerase. Compound 4a was found to be the most active with IC50 value of 14.8 mu M. In accordance with these results, compound 4a was screened for anti-cancer activity on liver cancer cell lines (Huh7, Mahlavu, HepG2, FOCUS). Compound 4a showed anti-cancer activity against Huh7 human hepatoma cell line with IC50 value of 4.29 mu M. Therefore, compound 4a could be considered as a new anti-cancer and anti-HCV lead compound.
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    Effect of etodolac hydrazone, a new compound synthesised from etodolac, on spermatozoon quality, testicular lipid peroxidation, apoptosis and spermatozoon DNA integrity
    (WILEY, 2016-03) SÜZGÜN, PELİN; Sariozkan, S.; Turk, G.; Cikla-Suzgun, P.; Guvenc, M.; Yuce, A.; Yay, A. H.; Canturk, F.; Kucukguzel, S. G.
    The aim of this study was to investigate the effect of etodolac hydrazone (EH), a new compound synthesised from etodolac, on spermatozoon quality, testicular lipid peroxidation, apoptosis and spermatozoon DNA integrity in rats. Group 1 (n=8) received 1ml dimethyl sulfoxide (DMSO) daily (Control); group 2 (n=8) was treated with 5mgkg(-1)day(-1) EH, dissolved in 1ml DMSO (EH-5); and group 3 (n=8) was treated with 10 mg kg(-1)day(-1) EH, dissolved in 1ml DMSO (EH-10). All administrations were performed by gavage and maintained for 8weeks. Both doses of EH administration caused significant decreases in absolute and relative weights of testis, whole epididymis, right cauda epididymis, and spermatozoon motility, spermatozoon count in comparison with the control group. Only 10mgkg(-1)day(-1) EH administration caused significant decreases in absolute and relative weights of seminal vesicles and serum testosterone level, and significant increases in testicular lipid peroxidation level, and numbers of TUNEL+ apoptotic germ cells and spermatozoa with damaged DNA along with some histopathological damages when compared to the control group. However, body and ventral prostate weight, and testicular antioxidant markers (glutathione, glutathione-peroxidase and catalase), were unaffected significantly by both doses of EH administration. In conclusion, two different doses of EH, in particular its high dose, damage to testicular spermatogenic cells and spermatozoon DNA and, it decreases spermatozoon motility, count and testosterone level in healthy rats.