Browsing by Author "Canpolat, Fuat Emre"

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Beneficial effects of nigella sativa oil on intestinal damage in necrotizing enterocolitis
(Taylor & Francis, 2012-10) Tayman, Cüneyt; Çekmez, Ferhat; Canpolat, Fuat Emre; Çetinkaya, Merih; Uysal, Sema; Tunç, Turan; Sarıcı, S. Ümit; Kafa, İlker Mustafa; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; 0000-0001-8309-0934; AAG-7125-2021; 8450193200
Aim: The aim of this study was to determine the beneficial effects of Nigella sativa oil (NSO) on rats with necrotizing enterocolitis (NEC). Material and Methods: Thirty newborn Sprague-Dawley rats were randomly divided into three groups as NEC, NEC + NSO, and control. NEC was induced by enteral formula feeding, exposure to hypoxia-hyperoxia and cold stress. Pups in the NEC + NSO group were administered NOS at a dose of 2 ml/kg daily by intraperitoneal route from the first day until the end of the study. Proximal colon and ileum were excised for histopathologic, apoptosis (TUNEL) and biochemical evaluation, including xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malonaldehyde (MDA), and myeloperoxdase (MPO) activities. Results: Pups in the NEC + NOS group had better clinical sickness scores and weight gain compared to the NEC group (p < 0.05). In the macroscopic assessment, histopathologic and apoptosis evaluation (TUNEL), severity of bowel damage was significantly lower in the NEC + NOS group compared to the NEC group (p < 0.05). Tissue GSH-Px and SOD levels were significantly preserved in the NEC + NSO group (p < 0.05), whereas, tissue MDA, MPO levels of the NEC + NSO group were significantly lower than those in the NEC group (p < 0.05). Conclusion: NSO significantly reduced the severity of intestinal damage in NEC.
CDP-choline reduces severity of intestinal injury in a neonatal rat model of necrotizing enterocolitis
(Academic Press Inc Elsevier Science, 2013-07) Çetinkaya, Merih; Çekmez, Ferhat; Canpolat, Fuat Emre; Uysal, Sema; Tunç, Turan; Sarıcı, Serdar Ümit; Cansev, Mehmet; Tayman, Cüneyt; Kafa, İlker Mustafa; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; M-9071-2019; AAG-7125-2021; 8872816100; 12243787300; 8450193200
Background: Cytidine 5'-diphosphocholine (CDP-choline) is an endogenous intermediate in the biosynthesis of phosphatidylcholine, a contributor to the mucosal defense of the intestine. The aim of this study was to evaluate the possible cytoprotective effect of CDP-choline treatment on intestinal cell damage, membrane phospholipid content, inflammation, and apoptosis in a neonatal rat model of necrotizing enterocolitis (NEC). Methods: We divided a total of 30 newborn pups into three groups: control, NEC, and NEC + CDP-choline. We induced NEC by enteral formula feeding, exposure to hypoxia-hyperoxia, and cold stress. We administered CDP-choline intraperitoneally at 300 mg/kg/d for 3 d starting from the first day of life. We evaluated apoptosis macroscopically and histopathologically in combination with proinflammatory cytokines in the gut samples. Moreover, we determined membrane phospholipid levels as well as activities of xanthine oxidase, superoxide dismutase, glutathione peroxidase, and myeloperoxidase enzymes and the malondialdehyde content of intestinal tissue. Results: Mean clinical sickness score, macroscopic gut assessment score, and intestinal injury score were significantly improved, whereas mean apoptosis score and caspase-3 levels were significantly reduced in pups in the NEC + CDP-choline group compared with the NEC group. Tissue proinflammatory cytokine (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) levels as well as tissue malondialdehyde content and myeloperoxidase activities were reduced, whereas glutathione peroxidase and superoxide dismutase activities were preserved in the NEC + CDP-choline group. In addition, NEC damage reduced intestinal tissue membrane phospholipids, whereas CDP-choline significantly enhanced total phospholipid and phosphatidylcholine levels. Long-term follow-up in additional experiments revealed increased body weight, decreased clinical sickness scores, and enhanced survival in CDP-cholineereceiving versus saline-receiving pups with NEC lesions. Conclusions: Our study reports, for the first time, beneficial effects of CDP-choline treatment on intestinal injury in a neonatal rat model of NEC. Our data suggest that CDP-choline may be used as an effective therapeutic agent to prevent NEC.
Cytidine 5 '-diphosphocholine ameliorates hyperoxic lung injury in a neonatal rat model
(Springernature, 2013-07) Çetinkaya, Merih; Tayman, Cüneyt; Çekmez, Ferhat; Canpolat, Fuat Emre; Tunç, Turan; Sarıcı, S. Ümit; Cansev, Mehmet; Kafa, İlker Mustafa; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; M-9071-2019; AAG-7125-2021; 8872816100; 8450193200
BACKGROUND: Bronchopulmonary dysplasia (BPD) is an important cause of morbidity. The aim of this study was to evaluate the preventive effect of cytidine 5'-diphosphocholine (CDP-choline) treatment on hyperoxic lung injury in a neonatal rat model. METHODS: A total of 30 newborn pups were divided into control, hyperoxia, and hyperoxia + CDP-choline groups. After birth, pups in the control group were kept in room air and received saline injections, whereas those in hyperoxia and hyperoxia + CDP-choline groups were exposed to 95% O-2 and received daily injections of saline and CDP-choline throughout postnatal day 10, respectively. Histopathological scoring, radial alveolar count, lamellar body membrane protein expression, fibrosis, proinflammatory cytokine levels, lung tissue and bronchoalveolar lavage (BAL) fluid phospholipid content, and apoptosis were evaluated. RESULTS: Hyperoxia-induced severe lung damage was reduced significantly by CDP-choline treatment. Radial alveolar count and lamellar body membrane protein expression were significantly recovered, and the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling-positive cells, active caspase-3 expression, and tissue proinflammatory cytokine levels were decreased by CDP-choline administration. Lung tissue and BAL phospholipid contents showed significant increases after COP-choline administration. CONCLUSION: These data show that COP-choline ameliorates hyperoxic lung injury in a neonatal rat model. It may therefore be suggested that CDP-choline may be a novel therapeutic option for the prevention of BPD.
Evaluation of melatonin and prostaglandin El combination on necrotizing enterocolitis model in neonatal rats
(Elsevier, 2013-06-10) Çekmez, Ferhat; Çetinkaya, Merih; Tayman, Cüneyt; Canpolat, Fuat Emre; Uysal, Sema; Tunç, Turan; Sarıcı, Serdar Ümit; Kafa, İlker Mustafa; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; AAG-7125-2021; 8450193200
Background: Necrotizing enterocolitis (NEC) is one of the most common gastrointestinal emergencies in newborn infants but up to now there is no completely effective treatment for it. Objective: In order to show that a combination of melatonin and prostaglandins may be useful to save lives, we use newborn rat as a model of necrotizing enterocolitis to test the hypothesis of using the combination therapy might have more potential effect on mucosal cytoprotection and healing. Patients and methods: A total of 60 newborn pups from 5 time-mated Sprague-Dawley pregnant rats were divided equally into 5 groups as follows: NEC (subjected to NEC), NEC + Melatonin, NEC + Prostaglandin, NEC + Prostaglandin + Melatonin and control. These animals were fed with hyperosmolar formula 3 times daily and subjected to 100% CO2 inhalation for 10 min, +4 degrees C cold exposure for 5 min, and 97% O-2 for 5 min twice daily to induce NEC. This procedure was applied to the pups for 3 days. Results: The macroscopic scoring, intestinal injury scoring and apoptosis index scoring were all found to be significantly lower in NEC + Prostaglandin + Melatonin group compared with NEC group. Anti-oxidant enzyme activities were significantly higher, whereas lipid peroxidation was significantly lower in NEC + Prostaglandin + Melatonin group compared with NEC group. Conclusion: This combination therapy showed cytoprotective and healing effects on mucosa in the intestinal tissue of rat pups in necrotizing enterocolitis model. Therefore, this therapy might also show benefit in preterm infants with NEC. After confirmation of this data by other clinical and experimental studies, it may be a novel therapeutic option for the prevention of NEC in preterm infants.
Protective effects of Nigella sativa Oil in hyperoxia-induced lung injury
(Elsevier, 2013-01) Tayman, Cüneyt; Çekmez, Ferhat; Canpolat, Fuat Emre; Çetinkaya, Merih; Tonbul, Alparslan; Uysal, Sema; Tunç, Turan; Sarıcı, Serdar Ümit; Kafa, İlker Mustafa; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; AAG-7125-2021; 8450193200
Background: Oxygen-induced lung injury is believed to lead to the development of bronchopulmonary dysplasia in premature infants. We have evaluated the beneficial effects of Nigella sativa oil (NSO) on rats with hyperoxia-induced lung injury. Methods: Thirty newborn Sprague-Dawley rats were randomly divided into 3 groups as hyperoxia (95% O-2), hyperoxia + NSO and control (21% O-2). Pups in the hyperoxia + NSO group were administered intraperitoneal NSO at a dose of 4 ml/kg daily during the study period. Histopathologic, immunochemical, and biochemical evaluations (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], malonaldehyde [MDA] and myeloperoxidase [MPO]) were performed. Results: In the histopathologic and immunochemical evaluation, severity of lung damage was significantly lower in the hyperoxia + NOS group (P<.05). Tissue GSH-Px and SOD levels were significantly preserved, and MDA, MPO levels were significantly lower in the hyperoxia + NSO group (P<.05). Conclusion: NSO significantly reduced the severity of lung damage due to hyperoxia.
Protective effects of valproic acid, a histone deacetylase inhibitor, against hyperoxic lung injury in a neonatal rat model
(Public Library Science, 2015-05-04) Cetinkaya, Merih; Cekmez, Ferhat; Tayman, Cuneyt; Canpolat, Fuat Emre; Kramer, Boris W.; Sarici, Serdar Umit; Cansev, Mehmet; Kafa, Ilker Mustafa; Yaylagul, Esra Orenlili; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; Uludağ Üniversitesi/Fen Edebiyat Fakültesi/Biyoloji Bölümü.; 0000-0003-2918-5064; 0000-0001-8309-0934; 0000-0002-5206-1185; M-9071-2019; AAG-7125-2021; ABH-4915-2020; 8872816100; 8450193200; 55618956600
Objective: Histone acetylation and deacetylation may play a role in the pathogenesis of inflammatory lung diseases. We evaluated the preventive effect of valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, on neonatal hyperoxic lung injury. Methods: Forty newborn rat pups were randomized in normoxia, normoxia+VPA, hyperoxia and hyperoxia+VPA groups. Pups in the normoxia and normoxia+VPA groups were kept in room air and received daily saline and VPA (30 mg/kg) injections, respectively, while those in hyperoxia and hyperoxia+VPA groups were exposed to 95% O2 and received daily saline and VPA (30 mg/kg) injections for 10 days, respectively. Growth, histopathological, biochemical and molecular biological indicators of lung injury, apoptosis, inflammation, fibrosis and histone acetylation were evaluated. Results: VPA treatment during hyperoxia significantly improved weight gain, histopathologic grade, radial alveolar count and lamellar body membrane protein expression, while it decreased number of TUNEL(+) cells and active Caspase-3 expression. Expressions of TGFβ3 and phospho-SMAD2 proteins and levels of tissue proinflammatory cytokines as well as lipid peroxidation biomarkers were reduced, while anti-oxidative enzyme activities were enhanced by VPA treatment. VPA administration also reduced HDAC activity while increasing acetylated H3 and H4 protein expressions. Conclusions: The present study shows for the first time that VPA treatment ameliorates lung damage in a neonatal rat model of hyperoxic lung injury. The preventive effect of VPA involves HDAC inhibition.