Yazar "Ozdamar, Emine Nur" seçeneğine göre listele

Listeleniyor 1 - 4 / 4
  • Küçük Resim Yok
    Yayın
    Angiotensin-converting enzyme inhibitor captopril ameliorates renal damage in a rat model of thermal injury
    (WALTER DE GRUYTER GMBH, 2013) Emekli-Alturfan, Ebru; Ozdemir, Gulsen; Saglam, Esra; Ozdamar, Emine Nur; Sehirli, Ozer; Sener, Goksel
    Background: Burn is a posttraumatic inflammatory condition accompanied by both local and distant effects leading to intense inflammation, tissue damage, and infection. Acute renal failure is a well-known complication of severe burns and is an important factor leading to an increase in mortality. Objective: To determine the effect of captopril treatment on renal damage in a rat model of thermal injury by evaluating oxidant antioxidant system parameters, sialic acid levels, glutathione-S-transferase (GST), and tissue factor (TF) activities. Methods: Under ether anesthesia, the shaved dorsum of the rats was exposed to a 90 degrees C water bath for 10 seconds to induce burn injury. Captopril (1 mg/kg) or saline was administered intraperitoneally immediately after, and at 24 hours after burn injury. Rats were decapitated at 48 hours following the burn injury and trunk blood was collected to assay blood urea nitrogen (BUN) and creatinine concentrations. To evaluate the presence of oxidant injury, kidney tissue samples were taken to determine malondialdehyde (MDA), glutathione (GSH), sialic acid levels, and the activities of superoxide dismutase (SOD), catalase, GST, and TF. In the sham group the same protocol was applied except that the dorstun was dipped in a 25 degrees C water bath for 10 seconds. Results: Severe skin scald injury (30% of total body surface area) caused significant decreases in GSH level, SOD and catalase activities, and significant increases in TF and GST activities, and sialic acid levels. Treatment of rats with captopril (1mg/kg) significantly elevated the reduced GSH levels, SOD and catalase activities, while it decreased MDA, sialic acid levels, GST and TF activities. Conclusions: The present study showed for the first time that, captopril scavenging of reactive free radicals, normalizing the activities of TF and GST seems to be a promising agent for restoring renal damage following thermal trauma.
  • Küçük Resim Yok
    Yayın
    Captopril protects against burn-induced cardiopulmonary injury in rats
    (TURKISH ASSOC TRAUMA EMERGENCY SURGERY, 2014) Saglam, Esra; Sehirli, Ahmet Ozer; Ozdamar, Emine Nur; Contuk, Gazi; Cetinel, Sule; Ozsavci, Derya; Suleymanoglu, Selami; Sener, Goksel
    BACKGROUND: This study was designed to determine the possible protective effect of captopril treatment against oxidative damage in heart and lung tissues induced by burn injury. METHODS: Under ether anesthesia, the shaved dorsum of Wistar albino rats was exposed to 90 C water bath for 10 seconds. Captopril was administered intraperitoneally (10 mg/kg) after the burn injury and repeated twice daily. In the sham group, the dorsum was dipped in a 25 C water bath for 10 seconds. At the end of the 24 hours, echocardiographic recordings were performed, then animals were decapitated and heart and lung tissue samples were taken for the determination of tumor necrosis factor-alpha (TNF-alpha) as a pro-inflammatory cytokine, malondialdehyde and glutathione levels and myeloperoxidase, caspase-3, and Na+, K+-ATPase activity in addition to the histological analysis. RESULTS: Burn injury caused significant alterations in left ventricular function. In heart and lung tissues, TNF-a and malondialdehyde levels and myeloperoxidase and caspase-3 activities were found to be increased, while glutathione levels and Na+, K+-ATPase activity were decreased due to burn injury. Captopril treatment significantly elevated the reduced glutathione level and Na+, K+-ATPase activity, and decreased cytokine and malondialdehyde levels and myeloperoxidase and caspase-3 activities. CONCLUSION: Captopril prevents burn-induced damage in heart and lung tissues and protects against oxidative organ damage.
  • Küçük Resim Yok
    Yayın
    The Effect of Captopril on Brain Apoptosis After Burn Injury in Rats
    (TURKISH NEUROSURGICAL SOC, 2013) Saglam, Ibrahim Yaman; Ozdamar, Emine Nur; Demiralay, Ebru; Sehirli, Ahmet Ozer; Sener, Goksel; Saglam, Esra
    AIM:The purpose of this study was to determine the possible protective effects of captopril treatment against apoptosis in the brain induced by burn injury. MATERIAL and METHODS: Under ether anaesthesia, Wistar albino rats (200-250 g) were exposed to a 900C (burn) or 250C (sham) water bath for 10 s. The ACE group was treated with i.p. 10 mg/kg captopril immediately after burn injury and this treatment was repeated twice daily. At the end of the 24 hour, brain samples were taken. Apoptotic brain cells marked by terminal deoxynucleotidyl transferase-mediated d-UTP-nick end labeling (TUNEL) were evaluated in the cerebellum and midbrain of rats. RESULTS: Apoptotic cells in the cerebellum were significantly decreased after captopril treatment and found to be lower when compared to the burn group (p<0.001). In the midbrain of rats, the numbers of TUNEL-positive cells and apoptotic bodies were significantly increased in the burn group when compared to the control group (p<0.001).The burn-induced changes were reduced in the captopril-treated burn group (p<0.01). CONCLUSION: Captopril has beneficial effects in burn injury and should be assessed as a therapeutic agent in the management of this condition.
  • Küçük Resim Yok
    Yayın
    nNOS expression in the brain of rats after burn and the effect of the ACE inhibitor captopril
    (ELSEVIER SCI LTD, 2013) Demiralay, Ebru; Saglam, Ibrahim Yaman; Ozdamar, Emine Nur; Sehirli, Ahmet Ozer; Sener, Goksel; Saglam, Esra
    Objective: To investigate the role of endogenous neuronal nitric oxide synthase (nNOS) on brain injury after burn and the effects of the captopril. Methods: Wistar albino rats (200-250 g) were exposed on the dorsal surface to 90 degrees C (burn) or 25 degrees C (sham) water for 10 s. The ACE group was treated with intraperitoneal 10 mg/kg captopril immediately after burn and this treatment was repeated twice daily. At the end of the 24 h brain samples were taken. nNOS was studied in brain areas by immunohistochemistry. Results: There was no difference between the cerebellar and hypothalamic areas the nNOS expression of all groups. nNOS expression increased in the frontal cortex, striatum and midbrain in the burn group compared to the control group. In the frontal cortex, nNOS expression significantly decreased after ACE inhibitor treatment (p < 0.05). The striatal nNOS of the ACE group significantly increased when compared to the control group (p = 0.001). In the midbrain of the animals, nNOS decreased in the ACE group. Hippocampal nNOS expression did not change after burn and significantly increased after ACE inhibitor therapy (p < 0.05). Conclusions: Our data showed that the pathophysiological events following burn appear to be related to an acute inflammatory reaction which is associated with nNOS in the frontal cortex, striatum and midbrain, and captopril treatment abrogates the nNOS response in the frontal cortex and midbrain. (C) 2012 Elsevier Ltd and ISBI. All rights reserved.