首页> 外文期刊>Inflammatory bowel diseases >Dietary Dunaliella bardawil, a beta-carotene-rich alga, protects against acetic acid-induced small bowel inflammation in rats.
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Dietary Dunaliella bardawil, a beta-carotene-rich alga, protects against acetic acid-induced small bowel inflammation in rats.

机译:膳食杜氏杜巴藻(Dunaliella bardawil)是一种富含β-胡萝卜素的藻类,可防止乙酸引起的大鼠小肠炎症。

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BACKGROUND: Reactive oxygen species mediate tissue injury in inflammatory bowel disease. Beta-carotene is known as a potent free radical quencher and antioxidant. AIM: The authors evaluated the efficacy of prefeeding Dunaliella bardawil, rich in beta-carotene, to ameliorate acid-induced enteritis in a rat model. METHODS: Enteritis was induced in female Sprague-Dawley rats by injection of 2 mL acetic acid (0.67 mol/L) to a ligated duodenal loop following 10 weeks of feeding diets containing beta-carotene and compared with various controls. The effects of beta-carotene were evaluated by changes in myeloperoxidase activity, histology, and histomorphometry. RESULTS: Feeding beta-carotene resulted in suppressed mucosal myeloperoxidase activity, both basal and that induced by acetic acid injection. Acetic acid treatment induced major histopathologic changes in the duodenal mucosa, including small, irregular, and distorted villi; damage to the epithelium; edema of the lamina propria; accumulation of inflammatory cells; and hemorrhage. Beta-carotene treatment prevented these acid-induced histopathologic changes, and this was confirmed by histomorphometry of the villi. CONCLUSIONS: These results demonstrate the effectiveness of beta-carotene in a rat model as a prophylactic dietary measure in reducing the effects of acid-induced enteritis and raise the possibility that patients with Crohn's disease may benefit from the consumption of natural beta-carotene.
机译:背景:活性氧介导炎症性肠病的组织损伤。 β-胡萝卜素被称为有效的自由基淬灭剂和抗氧化剂。目的:作者评估了预饲富含β-胡萝卜素的杜氏杜氏藻(Dunaliella bardawil)改善大鼠模型中酸诱导的肠炎的功效。方法:在喂食含β-胡萝卜素的食物10周后,通过向结扎的十二指肠环注射2 mL乙酸(0.67 mol / L),在雌性Sprague-Dawley大鼠中诱发肠炎,并与各种对照进行比较。 β-胡萝卜素的作用通过髓过氧化物酶活性,组织学和组织形态学的变化来评估。结果:饲喂β-胡萝卜素可抑制黏膜髓过氧化物酶的活性,无论是基础的还是由乙酸注射诱导的。乙酸治疗可引起十二指肠粘膜的主要组织病理学改变,包括小的,不规则的和扭曲的绒毛;对上皮的损害;固有层水肿;炎性细胞积聚;和出血。 β-胡萝卜素治疗阻止了这些酸诱导的组织病理学改变,绒毛的组织形态测定法证实了这一点。结论:这些结果证明了β-胡萝卜素在大鼠模型中作为预防性饮食措施的有效性,从而减少了酸诱导的肠炎的影响,并增加了克罗恩氏病患者可能受益于天然β-胡萝卜素的摄入的可能性。

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