Browsing by Author "Kucukler, Sefa"

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Effect of Chrysin on Methotrexate-Induced Testicular Damage in Rats
(Wiley, 2019) Belhan, Saadet; Comakli, Selim; Kucukler, Sefa; Gulyuz, Fetih; Yildirim, Serkan; Yener, Zabit
This study was conducted on 28 male Wistar albino rats to determine the effects of chrysin on methotrexate-induced damage to testicular tissue. Rats were grouped into four groups of seven rats reach: Group 1 (n = 7) was the control group to which no drugs were administered; this group was only provided with food and water. Group 2 (n = 7) was administered 20 mg/kg of methotrexate once intraperitoneally. Group 3 (n = 7) was administered 50 mg/kg of chrysin for 7 days orally. Group 4 (n = 7) was administered 20 mg/kg of methotrexate once intraperitoneally, followed by oral administration of 50 mg/kg of chrysin for 7 days. At the end of the experiment, rats were anaesthetised, rat testes were removed, and spermatozoon was obtained from the cauda epididymis. It was determined that sperm count and motility, glutathione peroxidase, superoxide dismutase and catalase activities decreased in the methotrexate group, whereas malondialdehyde, tumour necrosis factor-alpha, interleukin-1 beta and nuclear kappa factor B expression levels increased. Furthermore, damage to tubulus seminiferus structures and affusion in germ cells was identified. In the methotrexate + chrysin administered group, sperm count improved, biochemical enzyme levels increased, and structural improvements were observed in testicular tubules. These findings demonstrated that chrysin plays a protective role in testicular damage in rats.
Hepatoprotective Effects of Zingerone on Sodium Arsenite-Induced Hepatotoxicity in Rats: Modulating the Levels of Caspase-3/Bax Nlrp3/Nf-κb and Atf6/Ire1 Signaling Pathways
(Academic Press inc Elsevier Science, 2024) Eriten, Berna; Caglayan, Cuneyt; Gur, Cihan; Kucukler, Sefa; Diril, Halit
Objective: Long-term exposure to arsenic has been linked to several illnesses, including hypertension, diabetes, hepatic and renal diseases and cardiovascular malfunction. The aim of the current investigation was to determine whether zingerone (ZN) could shield rats against the hepatotoxicity that sodium arsenite (SA) causes. Methods: The following five groups of thirty-five male Sprague Dawley rats were created: I) Control; received normal saline, II) ZN; received ZN, III) SA; received SA, IV) SA + ZN 25; received 10 mg/kg body weight SA + 25 mg/kg body weight ZN, and V) SA + ZN 50; received 10 mg/kg body weight SA + 50 mg/kg body weight ZN. The experiment lasted 14 days, and the rats were sacrificed on the 15th day. While oxidative stress parameters were studied by spectrophotometric method, apoptosis, inflammation and endoplasmic reticulum stress parameters were measured by RT-PCR method. Results: The SA disrupted the histological architecture and integrity of the liver and enhanced oxidative damage by lowering antioxidant enzyme activity, such as those of glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) level and increasing malondialdehyde (MDA) level in the liver tissue. Additionally, SA increased the mRNA transcript levels of Bcl2 associated x (Bax), caspases (-3, -6, -9), apoptotic protease -activating factor 1 (Apaf-1), p53, tumor necrosis factor- alpha (TNF- alpha), nuclear factor kappa B (NF kappa B), interleukin-1 beta (IL-1 beta ), interleukin-6 (IL -6), c -Jun NH2-terminal kinase (JNK), mitogen-activated protein kinase 14 (MAPK14), MAPK15, receptor for advanced glycation endproducts (RAGE) and nod -like receptor family pyrin domain -containing 3 (NLRP3) in the liver tissue. Also produced endoplasmic reticulum stress by raising the mRNA transcript levels of activating transcription factor 6 (ATF-6), protein kinase RNA -like ER kinase (PERK), inositol-requiring enzyme 1 (IRE1), and glucose -regulated protein 78 (GRP-78). These factors together led to inflammation, apoptosis, and endoplasmic reticulum stress. On the other hand, liver tissue treated with ZN at doses of 25 and 50 mg/kg showed significant improvement in oxidative stress, inflammation, apoptosis and endoplasmic reticulum stress. Conclusions: Overall, the study ' s data suggest that administering ZN may be able to lessen the liver damage caused by SA toxicity.