The Journal of surgical research · 2015
Protective effects of butyrate on intestinal ischemia-reperfusion injury in 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.
Qiao Yingli, Qian Jianmin, Lu Qingyang, Tian Yaqiang, Chen Qi, Zhang Yang
Аннотация
BACKGROUND: Butyrate is normally fermented from undigested fiber by intestinal microflora. The goal of the present study was to determine the effects of butyrate and its underlying mechanisms on intestinal injury in a rat model of ischemia and reperfusion (I/R).
METHODS: Male Sprague-Dawley rats were subjected to warm ischemia for 45 min by clamping the superior mesenteric artery after treatment with butyrate, followed by 6 and 72 h of reperfusion. Pathologic histology analysis, enzyme-linked immunosorbent assay, immunofluorescence, and Western blot were performed.
RESULTS: Butyrate preconditioning markedly improved intestinal injury. The inflammatory factor levels and leukocyte infiltration were attenuated by butyrate. Butyrate also maintained the intestinal barrier structures, increased the expression of tight junction proteins, and decreased endotoxin translocation.
CONCLUSIONS: We conclude that butyrate administration attenuates intestinal I/R injury, which is associated with preservation of intestinal tight junction barrier function and suppression of inflammatory cell infiltration in the intestinal mucosa. This suggests butyrate as a potential strategy to prevent intestinal I/R injury.
METHODS: Male Sprague-Dawley rats were subjected to warm ischemia for 45 min by clamping the superior mesenteric artery after treatment with butyrate, followed by 6 and 72 h of reperfusion. Pathologic histology analysis, enzyme-linked immunosorbent assay, immunofluorescence, and Western blot were performed.
RESULTS: Butyrate preconditioning markedly improved intestinal injury. The inflammatory factor levels and leukocyte infiltration were attenuated by butyrate. Butyrate also maintained the intestinal barrier structures, increased the expression of tight junction proteins, and decreased endotoxin translocation.
CONCLUSIONS: We conclude that butyrate administration attenuates intestinal I/R injury, which is associated with preservation of intestinal tight junction barrier function and suppression of inflammatory cell infiltration in the intestinal mucosa. This suggests butyrate as a potential strategy to prevent intestinal I/R injury.