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Öğe Effects of Curcumin on Apoptosis and Oxidoinflammatory Regulation in a Rat Model of Acetic Acid-Induced Colitis: The Roles of c-Jun N-Terminal Kinase and p38 Mitogen-Activated Protein Kinase(Mary Ann Liebert, Inc, 2013) Topcu-Tarladacalisir, Yeter; Akpolat, Meryem; Uz, Yesim Hulya; Kizilay, Gulnur; Sapmaz-Metin, Melike; Cerkezkayabekir, Aysegul; Omurlu, Imran KurtThe present study evaluated the effects of curcumin on epithelial cell apoptosis, the immunoreactivity of the phospho-c-Jun N-terminal kinase (JNK) and phospho-p38 mitogen-activated protein kinases (MAPKs) in inflamed colon mucosa, and oxidative stress in a rat model of ulcerative colitis induced by acetic acid. Rats were randomly divided into three groups: control, acetic acid, and acetic acid + curcumin. Curcumin (100 mg/kg per day, intragastrically) was administered 10 days before the induction of colitis and was continued for two additional days. Acetic acid-induced colitis caused a significant increase in the macroscopic and microscopic tissue ranking scores as well as an elevation in colonic myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, and the number of apoptotic epithelial cells in colon tissue compared to controls. In the rat colon, immunoreactivity of phospho-p38 MAPK was increased, whereas the phospho-JNK activity was decreased following the induction of colitis. Curcumin treatment was associated with amelioration of macroscopic and microscopic colitis sores, decreased MPO activity, and decreased MDA levels in acetic acid-induced colitis. Furthermore, oral curcumin supplementation clearly prevented programmed cell death and restored immunreactivity of MAPKs in the colons of colitic rats. The results of this study suggest that oral curcumin treatment decreases colon injury and is associated with decreased inflammatory reactions, lipid peroxidation, apoptotic cell death, and modulating p38- and JNK-MAPK pathways.Öğe Investigation of the Protective Effects of Proanthocyanidin and Vitamin E against the Toxic Effect caused by Formaldehyde on the Liver Tissue(Wiley-Blackwell, 2015) Bakar, Elvan; Ulucam, Enis; Cerkezkayabekir, AysegulWe aimed to investigate of protective role of proanthocyanidin (PA) and vitamin E (vit E) against to toxic effect of formaldehyde (FA). Twenty-eight Wistar albino rats were divided into four groups: control group, rats treated with FA intraperitoneal (i.p.) (10 mg/kg), FA + vit E intragastric (i.g.) (30 mg/kg), and FA + PA i.g. (100 mg/kg). We assayed superoxide dismutase (SOD), glutathione peroxidase (Gpx), myeloperoxidase (MPO) activity and levels of malondialdehyde (MDA) and total sialic acid (TSA) in liver. Liver tissue was taken in order to morphological analysis and hepatocytes apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay immunostaining. SOD decreased in FA and increased in FA + vit E and FA + PA (p < 0.05). Gpx didn't change in FA and increased in FA + PA (p < 0.05). No significant variation between the groups was found in MPO activity. MDA increased only in FA and decreased in FA + vit E and FA + PA (p < 0.05). TSA didn't alter in FA and FA + vit E but decreased in FA + PA (p < 0.05). Degeneration in hepatocytes and endothelial cells, cytoplasm losses, vacuolization, picnotic nuclei, and mononuclear cell infiltration were identified in FA. Degeneration in chromatin material, membrane damage in mitochondria and losses in mitochondrial cristae in hepatocytes were observed in FA. We found that partially recovery in liver as a result of FA + vit E and FA + PA. We have concluded that long term use should be investigated for complete explanation of PA's protective effects on FA toxicity. (C) 2014 Wiley Periodicals, Inc.Öğe N-acetylcysteine counteracts oxidative stress and protects alveolar epithelial cells from lung contusion-induced apoptosis in rats with blunt chest trauma(Springer, 2014) Topcu-Tarladacalisir, Yeter; Tarladacalisir, Taner; Sapmaz-Metin, Melike; Karamustafaoglu, Altemur; Uz, Yesim Hulya; Akpolat, Meryem; Cerkezkayabekir, AysegulThe aim of this study was to investigate the protective effects of N-acetylcysteine (NAC) on peroxidative and apoptotic changes in the contused lungs of rats following blunt chest trauma. The rats were randomly divided into three groups: control, contusion, and contusion + NAC. All the rats, apart from those in the control group, performed moderate lung contusion. A daily intramuscular NAC injection (150 mg/kg) was given immediately following the blunt chest trauma and was continued for two additional days following cessation of the trauma. Samples of lung tissue were taken in order to evaluate the tissue malondialdehyde (MDA) level, histopathology, and epithelial cell apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and active caspase-3 immunostaining. In addition, we immunohistochemically evaluated the expression of surfactant protein D (SP-D) in the lung tissue. The blunt chest trauma-induced lung contusion resulted in severe histopathological injury, as well as an increase in the MDA level and in the number of cells identified on TUNEL assay together with active caspase-3 positive epithelial cells, but a decrease in the number of SP-D positive alveolar type 2 (AT-2) cells. NAC treatment effectively attenuated histopathologic, peroxidative, and apoptotic changes, as well as reducing alterations in SP-D expression in the lung tissue. These findings indicate that the beneficial effects of NAC administrated following blunt chest trauma is related to the regulation of oxidative stress and apoptosis.Öğe Role of JNK, TGF-?1, Akt, IL-1? and INSL-3 in proanthocyanidin protection against apoptosis in diabetic rat testis(Taylor & Francis Ltd, 2022) Kizilay, Gulnur; Bayram, Sinasi; Ersoy, Onur; Cerkezkayabekir, Aysegul; Sapmaz-Metin, Melike; Karaca, TuranWe investigated how proanthocyanidin treatment altered c-Jun N-terminal kinases, transforming growth factor beta 1, serine/threonine-specific protein kinase, interleukin 1 beta and insulin-like 3 expression in the testis of diabetic rats. We used 24 Wistar albino male rats divided into four groups. Group 1 was untreated control. Group 2 was treated with 40 mg/kg streptozotocin (STZ) for 5 days. Group 3 was treated with 40 mg/kg STZ + 250 mg/kg proanthocyanidin once daily for six weeks. Group 4 was treated with 40 mg/kg STZ + 250 mg/kg proanthocyanidin. Superoxide dismutase activity was reduced in groups 3 and 4 compared to group 2. Glutathione peroxidase activity was increased significantly in groups 3 and 4 compared to groups 1 and 2. Catalase activity was decreased in group 4 compared to group 2. We found that proanthocyanidin increased cell proliferation in diabetic testis. Phospho-JNK and TGF-beta 1 immunostaining was decreased groups 3 and 4 compared to group 2, while p-Akt immunostaining was increased in groups 3 and 4. The number of IL-1 beta immunostained cells in groups 3 and 4 was decreased compared to group 2. INSL-3 immunostaining was increased significantly in group 3 compared to group 2. Our findings indicate that proanthocyanidin ameliorated diabetes related testicular dysfunction. Proanthocyanidin contributes to a balanced oxidant-antioxidant status, and balanced proliferation and apoptosis activity in the germinal cells.Öğe Sitagliptin and fucoidan prevent apoptosis and reducing ER stress in diabetic rat testes(Wiley, 2021) Kizilay, Gulnur; Ersoy, Onur; Cerkezkayabekir, Aysegul; Topcu-Tarladacalisir, YeterSitagliptin increases the levels of incretin hormones and stimulates a decrease in blood glucose levels, by blocking the DPP4 enzyme. We have very limited information about impact of sitagliptin on male genital system and relationship between sitagliptin/diabetes/ER. Fucoidan can be effective in blood glucose homeostasis. We goal to explain of the effect of sitagliptin and introduce an approach of fucoidan treatment in experimental diabetes in male rats. Fifty-eight Wistar albino rats were divided into C-control group and D-diabetes group: 60 mg/kg streptozotocin intraperitoneal (i.p.); DS group: STZ + 10 mg/kg sitagliptin intragastric (i.g.); DF group: STZ + 100 mg/kg fucoidan i.p.; and DSF group: STZ + 10 mg/kg sitagliptin + 100 mg/kg fucoidan. A significant decrease was detected when DS, DF and DSF groups compared to group D in blood glucose levels, basement membrane thickness and also apoptotic cell/tubule index, pJNK, caspase 3, caspase 12, GRP78, CHOP and DPP4. Sitagliptin and fucoidan have been found to be effective in blood glucose homeostasis and reducing the expression of certain proteins that lead to apoptosis and especially the proteins in the ER stress pathway. Therefore, we think that both sitagliptin and fucoidan can be effective in preventing or eliminating histopathological damages in diabetic testicular tissues, and their treatment effects can be used more.Öğe Ultrastructural changes in rat liver by methyleugenol and evaluation of some biochemical parameters(Tubitak Scientific & Technological Research Council Turkey, 2010) Cerkezkayabekir, Aysegul; Kizilay, Gulnur; Ertan, FigenThe present study investigated the effect of methyleugenol, a food flavoring and fragrance agent, on the livers of laboratory rats. Doses of 10 and 30 mg/kg/day of methyleugenol (in 0.5% methylcellulose) were administered intragastrically (IG) to 2 dose groups for 10 days alongside a control group (n = 10 for each group). Gains in body weight were not statistically significant for either dose. Lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) activities decreased (P < 0.05) for both dose groups, but AST (aspartate aminotransferase) activity decreased significantly (P < 0.05) only in the 30 mg/kg/day methyleugenol dose group. Alanine aminotransferase (ALT) activity did not change significantly in either group. The total amount of glucose remained unchanged, but glycogen in the liver decreased significantly (P < 0.05) in the 30 mg/kg/day methyleugenol dose group. There was also an increase of swelling in the smooth endoplasmic reticulum sacs (sER), electron dense accumulations in the sER, cytoplasmic vacuolization, a slight increase of mitochondria and lysosomes, and invaginations in the nucleus membranes of hepatocytes. Extensions in bile canaliculi and increasing microvilli of bile canaliculi in the liver were also observed. These findings indicate the ultrastructural toxic effect of methyleugenol on rat livers in 10 and 30 mg/kg/day doses. Therefore, we may speculate that the toxic effect of methyleugenol needs to be examined in detail.Öğe Vitamin E modulates apoptosis and c-jun N-terminal kinase activation in ovarian torsion-detorsion injury(Academic Press Inc Elsevier Science, 2013) Sapmaz-Metin, Melike; Topcu-Tarladacalisir, Yeter; Uz, Yesim Hulya; Inan, Mustafa; Omurlu, Imran Kurt; Cerkezkayabekir, Aysegul; Kizilay, GulnurThe aim of this study was to evaluate the role of vitamin E in follicular degeneration and to assess histopathological and biochemical changes following ischemia-reperfusion (IR) injury in rat ovaries. Twenty-eight Wistar albino rats were randomly divided into four groups: sham, 4 h torsion, 24 h detorsion, and a vitamin E group. Thirty minutes before detorsion, a single dose of 200 mg/kg vitamin E was administered intraperitoneally. The ovarian histology score was determined, serum levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were measured. The apoptosis of granulosa cells and the phospho-c-jun N-terminal kinase (p-JNK) and phospho-p38 (p-p38) immunoreactivities of these cells were determined. MDA and MPO levels were significantly increased in the torsion and detorsion groups. Hemorrhage, edema, and congestion were also apparent in these groups. In addition, the apoptotic index and the immunoreactivity of p-JNK were highest in the detorsion group, which also showed marked follicular degeneration. However, p-p38 activity was not affected by torsion-detorsion (TD) induction. Vitamin E ameliorated TD-induced histological alterations. It also decreased serum levels of MDA and MPO, reduced the activity of p-JNK in the ovaries, and reduced numbers of apoptotic follicular cells. In conclusion, these data indicate that vitamin E attenuated ovarian follicular degeneration by inhibiting the immunoreactivity of p-JNK and reducing the apoptosis of granulosa cells. (c) 2013 Elsevier Inc. All rights reserved.
