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Kidney damage due to ischemia-reperfusion injury (IRI) is a serious cause of morbidity and mortality. We induced an experimental kidney ischemia-reperfusion model in rats where intraperitoneal dexpanthenol were given and compared to controls in terms of oxidative stress, tubular damage, apoptosis, and its effect on renal inflammation.Twelve-week-old male albino Wistar rats were used for creating the experimental model and the study sample were divided into three groups (n=16); control group (intraperitoneal 2cc/kg saline was injected), IRI group and IRI+dexpanthenol group via intraperitoneal injection. Blood samples were obtained from rats 24 hours after perfusion and their left kidneys were removed. In order to determine the percentage of apoptotic cells, a total of 100 cells were counted in each region and the number of cells with caspase-3 positivity was recorded for each region. Mortality was lower, although not statistically significant in the IRI+dexpanthenol group (n=3; 18.8%) compared to the IRI group (n=6; 37.5%) (p=0.216). In addition, kidney parenchyma and tubular damages were significantly lower in the dexpanthenol group compared to the IRI group (p Abstract Kidney damage due to ischemia-reperfusion injury (IRI) is a serious cause of morbidity and mortality. We induced an experimental kidney ischemia-reperfusion model in rats where intraperitoneal dexpanthenol were given and compared to controls in terms of oxidative stress, tubular damage, apoptosis, and its effect on renal inflammation.Twelve-week-old male albino Wistar rats were used for creating the experimental model and the study sample were divided into three groups (n=16); control group (intraperitoneal 2cc/kg saline was injected), IRI group and IRI+dexpanthenol group via intraperitoneal injection. Blood samples were obtained from rats 24 hours after perfusion and their left kidneys were removed. In order to determine the percentage of apoptotic cells, a total of 100 cells were counted in each region and the number of cells with caspase-3 positivity was recorded for each region. Mortality was lower, although not statistically significant in the IRI+dexpanthenol group (n=3; 18.8%) compared to the IRI group (n=6; 37.5%) (p=0.216). In addition, kidney parenchyma and tubular damages were significantly lower in the dexpanthenol group compared to the IRI group (p Özet İskemi-reperfüzyon injürisine (IRI) bağlı böbrek hasarı ciddi bir morbidite ve mortalite nedenidir. İntraperitoneal dekspantenol verilen ratlarda deneysel bir böbrek iskemi-reperfüzyon modeli oluşturduk ve oksidatif stres, tübüler hasar, apoptoz ve renal inflamasyon üzerindeki etkisi açısından kontrollerle karşılaştırdık. Deneysel modelin oluşturulmasında 12 haftalık erkek albino Wistar ratlar kullanıldı ve çalışma örneklemi 3 gruba ayrıldı (n=16); kontrol grubu (intraperitoneal 2cc/kg salin enjekte edildi), IRI grubu ve intraperitoneal enjeksiyon uygulaması ile oluşturulan IRI+dekspantenol grubu. Perfüzyondan 24 saat sonra ratlardan kan örnekleri toplandı ve sol böbrekleri alındı. Apoptotik hücre yüzdesini belirlemek için her bölgede toplam 100 hücre sayıldı ve her bölge için kaspaz-3 pozitifliği olan hücre sayısı kaydedildi. Mortalite IRI+dekspantenol grubunda (n=3; 18.8), IRI grubuna (n=6; %37.5) göre istatistiksel olarak anlamlı düzeyde olmamakla beraber daha düşüktü(p=0.216). Ayrıca böbrek parankimi ve tübüler hasarlar dekspantenol grubunda IRI grubuna göre anlamlı olarak daha düşüktü (p |
