Person: ALKAN, TÜLİN
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ALKAN
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TÜLİN
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Publication Effects of short-term uridine treatment on blood-brain barrier integrity and brain edema in li-pilocarpine-induced status epilepticus(Wiley, 2023-01-01) Aydın, Birnur; Esmerce, Buşra Öcalan; ÇAKIR, AYŞEN; ESMERCE, BÜŞRA; KOÇ, CANSU; Koç, Cansu; Tuncak, Şüeda; TUNÇAK, SÜEDA; Cansev, Mehmet; CANSEV, MEHMET; Alkan, Tulin; ALKAN, TÜLİN; AAH-1792-2021; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; 0000-0002-8193-474X; 0000-0003-2918-5064; 0000-0001-6466-5042; LFV-6689-2024; M-9071-2019; A-6819-2018; AAH-1734-2021; AAH-1734-2021; A-6819-2018; LFV-6689-2024; AAH-1792-2021Publication Preventive effects of maternal CDP-choline, administered either alone or in combination with a steroid, on lung injury in a neonatal rat model of hyperoxia(Springernature, 2019-09-01) Koç, Cansu; Cansev, Mehmet; Alkan, Tülin; Kafa, İlker Mustafa; Çetinkaya, Merih; KOÇ, CANSU; CANSEV, MEHMET; ALKAN, TÜLİN; KAFA, İLKER MUSTAFA; Bursa Uludağ Üniversitesi/Tıp Fakültesi.; 0000-0001-8309-0934; AAA-4754-2022; M-9071-2019; AAH-1792-2021; AAG-7125-2021Publication Antioxidative effects of uridine in a neonatal rat model of hyperoxic brain injury(TÜBİTAK, 2020-05-31) Al, Nevin; Çakir, Aysen; Koç, Cansu; Cansev, Mehmet; Alkan, Tülin; ÇAKIR, AYŞEN; KOÇ, CANSU; CANSEV, MEHMET; ALKAN, TÜLİN; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; 0000-0002-6097-5585; 0000-0003-2918-5064; 0000-0001-6466-5042; AAA-4754-2022; A-6819-2018; M-9071-2019; AAH-1792-2021Background/aim: Premature birth is a major problem that results in an increased risk of mortality and morbidity. The management of such infants consists of supraphysiological oxygen therapy, which affects brain development due, in part, to the deterioration caused by reactive oxygen species (ROS). We showed previously that exogenously administered uridine provides neuroprotection in a neonatal rat model of hyperoxic brain injury. Hence, the aim of the present study was to investigate the effects of uridine on ROS in the same setting.Materials and methods: Hyperoxic brain injury was induced by subjecting a total of 53 six-day-old rat pups to 80% oxygen (the hyperoxia group) for a period of 48 h. The pups in the normoxia group continued breathing room air (21% oxygen). Normoxia + saline or hyperoxia + saline or hyperoxia + uridine 100 mg/kg or hyperoxia + uridine 300 mg/kg or hyperoxia + uridine 500 mg/kg was injected intraperitoneally (i. p.) 15 min prior to the hyperoxia procedure. The pups were decapitated and the brains were homogenized to analyze superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), and malondialdehyde (MDA) enzymes as well as DJ-1 (protein deglycase DJ-1) - an oxidative stress-sensitive protein.Results: Hyperoxia-induced may cause overproduction of oxygen radicals and the oxidant/antioxidant balance may be disturbed in the brain. Brain MPO and MDA levels were significantly increased in saline-receiving pups exposed to hyperoxia. Brain SOD and GSH-Px levels were significantly decreased in saline-receiving pups exposed to hyperoxia. Our results showed that uridine administration prevented the hyperoxia-induced decrease in SOD and GSH-Px while counteracting the hyperoxia-induced increase in MPO and MDA in a dose-dependent manner. Uridine also increased the DJ-1 levels in brains of rat pups subjected to hyperoxia.Conclusion: These data suggest that uridine exhibits antioxidative properties which may mediate the protective effects of uridine in a neonatal rat model of hyperoxic brain injury.Publication Preventive effects of antenatal CDP-choline in a rat model of neonatal hyperoxia-induced lung injury(Canadian Science Publishing, 2022-12-16) Koç, Cansu; Çakır, Ayşen; Salman, Berna; Öcalan, Büşra; Alkan, Tülin; Kafa, Ilker Mustafa; Çetinkaya, Merih; Cansev, Mehmet; KOÇ, CANSU; ÇAKIR, AYŞEN; SALMAN, BERNA; Öcalan, Büşra; ALKAN, TÜLİN; KAFA, İLKER MUSTAFA; CANSEV, MEHMET; Bursa Uludağ ÜniversitesiTıp Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.; 0000-0001-8309-0934; 0000-0002-6097-5585; A-6819-2018; N-9927-2019; AAH-1792-2021; LGY-8580-2024; M-9071-2019; AAG-7125-2021; DQU-6929-2022Antenatal steroid administration to pregnant women at risk of prematurity provides pulmonary maturation in infants, while it has limited effects on incidence of bronchopulmonary dysplasia (BPD), the clinical expression of hyperoxia-induced lung injury (HILI). Cytidine-5'-diphosphate choline (CDP-choline) was shown to alleviate HILI when administered to newborn rats. Therefore, we investigated effects of maternal administration of CDP-choline, alone or in combination with betamethasone, on lung maturation in neonatal rats subjected to HILI immediately after birth. Pregnant rats were randomly assigned to one of the four treatments: saline (1 mL/kg), CDP-choline (300 mg/kg), betamethasone (0.4 mg/kg), or CDP-choline plus betamethasone (combination therapy). From postnatal day 1 to 11, pups born to mothers in the same treatment group were pooled and randomly assigned to either normoxia or hyperoxia group. Biochemical an d histopathological effects of CDP-choline on neonatal lung tissue were evaluated. Antenatal CDP-choline treatment increased levels of phosphatidylcholine and total lung phospholipids, decreased apoptosis, and improved alveolarization. The outcomes were further improved with combination therapy compared to the administration of CDP-choline or betamethasone alone. These results demonstrate that antenatal CDP-choline treatment provides benefit in experimental HILI either alone or more intensively when administered along with a steroid, suggesting a possible utility for CDP-choline against BPD.