J. Malago, K. Omar, M. Mwangwa, M. Isaac, As Msengwa
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引用次数: 0
摘要
由于短链脂肪酸对健康有益,它们越来越多地被用作食品添加剂。最近,它们与保护患者免受肠道疾病的影响有关,但没有一个众所周知的机制。我们探讨了一种主要的短链脂肪酸,丁酸酯对实验性大鼠溃疡性结肠炎的益处。溃疡性结肠炎是在暴露于乙酸前连续3天分别腹腔或直肠内分别给予50或150 mg/kg丁酸后或未事先给予丁酸后,通过直肠内滴注10%乙酸诱导的。大鼠暴露于醋酸24h后处死,尸检,固定肠切片,常规处理及组织病理学染色。醋酸诱导炎症细胞浸润,上皮细胞丢失,隐窝损伤,结肠杯状细胞丢失。这些变化在丁酸盐处理后被显著抑制。我们得出结论,丁酸盐降低了大鼠醋酸诱导的溃疡性结肠炎病变的严重程度。这种保护效力可能是,至少在一定程度上,通过丁酸盐赋予其溃疡性结肠炎患者的好处的机制之一。坦桑尼亚兽医杂志Vol. 25 (1) 2008: pp. 1-12
Butyrate Suppresses The Severity Of Acetic Acid-Induced Ulcerative Colitis In Rats
Short chain fatty acids are increasingly used as food additives due to the health benefits they have. Recently, they have been implicated in protecting patients against intestinal disorders but without a well-known mechanism. We explored the benefits of a major short chain fatty acid, butyrate on experimental ulcerative colitis in rats. The ulcerative colitis was induced by intrarectal instillation of 10% acetic acid after or without prior administration of 50 or 150 mg/kg butyrate intraperitoneally or intrarectally, respectively, for three consecutive days prior to exposure to acetic acid. After 24 hours of
exposure to acetic acid, rats were sacrificed, postmortem examination done, intestinal sections fixed, processed and stained for histopathology in a routine manner. Acetic acid induced infiltration of inflammatory cells, loss of epithelium, crypt damage, and loss of goblet cells in the colon. These changes were significantly suppressed following butyrate treatment. We conclude that butyrate reduces the severity of acetic acid induced ulcerative colitis lesions in rats. This protective potency could be, at least in part, one of the mechanisms by which butyrate imparts its benefits to ulcerative colitis patients. Tanzania Veterinary Journal Vol. 25 (1) 2008: pp. 1-12