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    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.
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    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.