Intensive care medicine · 2006
The effect of melatonin on endotoxemia-induced intestinal apoptosis and oxidative stress in infant rats.
Оценочное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ozdemir Durgul, Uysal Nazan, Tugyan Kazim, Gonenc Sevil, Acikgoz Osman, Aksu Ilkay, Ozkan Hasan
Аннотация
OBJECTIVE: To evaluate the effect of melatonin on the intestinal apoptosis along with oxidative damage in endotoxemic infant rats.
DESIGN AND SETTING: Prospective animal study in a university-based experimental research laboratory.
SUBJECTS AND INTERVENTIONS: Wistar albino 7-day-old rat pups (n=21). The animals were randomized into three experimental groups: (1) controls; (2) endotoxemia; (3) endotoxemia treated with melatonin (10mg/kg). Endotoxemia was induced in rats by intraperitoneal injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 3 mg/kg).
MEASUREMENTS AND RESULTS: Four hours after LPS injection, the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substance (TBARS) levels as an indicator of lipid peroxidation, were determined. Intestinal apoptosis was assessed by hematoxylin-eosin staining and terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling. The administration of melatonin into endotoxemic rats prevented the increase in the TBARS levels, and increased the activities of antioxidant enzymes and attenuated apoptotic cell death in both intestinal epithelium and lamina propria.
CONCLUSIONS: Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infant rats.
DESIGN AND SETTING: Prospective animal study in a university-based experimental research laboratory.
SUBJECTS AND INTERVENTIONS: Wistar albino 7-day-old rat pups (n=21). The animals were randomized into three experimental groups: (1) controls; (2) endotoxemia; (3) endotoxemia treated with melatonin (10mg/kg). Endotoxemia was induced in rats by intraperitoneal injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 3 mg/kg).
MEASUREMENTS AND RESULTS: Four hours after LPS injection, the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substance (TBARS) levels as an indicator of lipid peroxidation, were determined. Intestinal apoptosis was assessed by hematoxylin-eosin staining and terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling. The administration of melatonin into endotoxemic rats prevented the increase in the TBARS levels, and increased the activities of antioxidant enzymes and attenuated apoptotic cell death in both intestinal epithelium and lamina propria.
CONCLUSIONS: Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infant rats.