Protective effect of dietary nitrate on experimental gastritis in rats
Protective effect of dietary nitrate on experimental gastritis in rats
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DOI：
10.1079/bjn2003845
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发表时间：
2003-06-01
影响因子：
3.6
通讯作者：
Fioramonti, J
中科院分区：
文献类型：
--
作者：
Larauche, M;Anton, PM;Fioramonti, J
长期以来，硝酸盐一直被认为是有害的膳食成分，并被认为对人类健康造成有害影响，导致对其在食品和水中的含量进行严格的规定。然而，最近的研究表明，膳食硝酸盐可能在人体健康中发挥重要作用，作为宿主防御的非免疫机制，通过其在胃中代谢为NO。NO是一种多功能分子，尽管有证据表明给予低剂量的外源性NO可保护胃肠道炎症，但已显示较高的NO剂量会加剧损伤。因此，研究了摄入相当于人类消费者正常饮食剂量的硝酸盐对大鼠碘乙酰胺诱导的实验性胃炎的影响。在胃炎期间，口服以下化合物之一：水; KNO 3; NO供体硝酸锌钠;与水或KNO 3一起给予的NO清除剂血红蛋白。N（G）-体外-L-精氨酸甲酯（L-NAME）是一种非特异性NO合成酶抑制剂，与水、碘乙酰胺单独或与NO 3联合给药。处死后，切除胃并测定显微镜损伤评分、髓过氧化物酶和NO合酶活性。碘乙酰胺诱导的胃炎显着减少硝酸钾管理，这是由硝普钠复制和血红蛋白逆转的效果。L-NAME本身可引起胃粘膜损伤，KNO 3不能阻止L-NAME联合碘乙酰胺引起的胃炎。总之，膳食中的硝酸盐通过在胃中释放NO对大鼠实验性胃炎具有保护作用，但这种作用需要内源性NO的产生。
Nitrates have long been considered as harmful dietary components and judged responsible for deleterious effects on human health, leading to stringent regulations concerning their levels in food and water. However, recent studies demonstrate that dietary nitrate may have a major role in human health as anon-immune mechanism for host defence, through its metabolism to NO in the stomach. NO is a versatile molecule and although evidence exists showing that administration of low doses of exogenous NO protects against gastrointestinal inflammation, higher NO doses have been shown to exacerbate injury. So, the effect of an ingestion of nitrates in doses corresponding to a normal diet in human consumers on an experimental gastritis induced by iodoacetamide in rats was investigated. During gastritis one of the following compounds as given orally: water; KNO3; the NO donor sodium nitcoprusside; the NO scavenger haemoglobin given with either water or KNO3. N(G)-vitro-L-arginine methyl ester (L-NAME), a non-specific NO, synthase inhibitor, was administered with-either water, iodoacetamide alone, or combined with NO3. After killing, the stomach was resected and microscopic damage scores, myeloperoxidase and NO synthase activities were determined. Iodoacetanude-induced gastritis was significantly reduced by KNO3 administration, an effect which was reproduced by sodium nitroprusside and reversed by haemoglobin. L-NAME induced gastric mucosal damage in itself and KNO3 did not prevent the gastritis induced by iodoacetamide associated with L-NAME. In conclusion, dietary, nitrate exerts-a protective effect against an experimental gastritis in rats by releasing NO in the stomach but such an effect requires the production of endogenous NO.