Publication: The Effect of Captopril on Brain Apoptosis After Burn Injury in Rats
Abstract
AMAÇ: Yanığın indüklediği, beyinde meydana gelen apoptozise karşı kaptoprilin koruyucu etkisini araştırmak amaçlanmıştır. YÖNTEM ve GEREÇLER: Anestezi altındaki Wistar albino sıçanlar (200-250 g) 900C (yanık) ya da 250C (sham-kontrol) su buharına 10 dakika süresince tutuldu. Sıçanlar, yanık oluşumunu takiben i.p. 10 mg/kg kaptopril ile günde iki kez olmak üzere tedavi edildi. Serebellum ve orta beyinden çıkarılan hücrelerde apoptozun saptanmasında terminal deoxynucleotidyl transferase- mediated d-UTP- (TUNEL) yöntemi kullanıldı. BULGULAR: Yanık grubu ve sham-kontrol grubu serebellum bölgesinde oluşmuş olan apoptotik hücre sayısı açısından karşılaştırıldığında, TUNEL-positif apoptotik hücre sayısı yanık grubunda anlamlı olarak artmış bulundu (p<0.001). Serebellumdaki apoptotik hücre sayısının, kaptopril tedavisinden sonra, yanık grubu ile karşılaştırıldığında anlamlı olarak azaldığı görüldü (p<0.001). Ortabeyinde ise, apoptotik TUNEL- positif hücre sayısı yanık ve kontrol grubu karşılaştırıldığında, yanık grubunda anlamlı olarak arttığı gözlendi (p<0.001), yanığın indüklediği apoptotik değişiklikler ise kaptopril tedavisi ile anlamlı olarak azaldı (p<0.01). SONUÇ: Kaptopril yanık hasarı ile beyinde meydana gelen apoptotik değişiklikleri geri döndürmüştür. Yanık hasarının tedavisinde faydalı bir ilaç olabilir.
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 hours, 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.
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 hours, 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.