NITRIC OXIDE IN CHRONIC COLITIS OF MACAQUES

猕猴慢性结肠炎中的一氧化氮

• 批准号: 3742079
• 负责人: NICHOLAS W LERCHE
• 金额: --
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3742079
• 关键词: Macaca mulatta; colitis; colon; gene expression; histochemistry /cytochemistry; inflammation; juvenile animal; nitric oxide; nitric oxide synthase; polymerase chain reaction

The role of nitric oxide (NO) in the pathogenesis of chronic idiopathic colitis was assessed in juvenile rhesus macaques. The site, enzyme source and magnitude of no production was determined in juvenile rhesus diagnosed with chronic colitis/diarrhea, and scheduled for euthanasia. No production was evaluated systemically from plasma and urine levels of reactive nitrogen intermediates, and locally in the colon by NADPH diaphorase histochemistry. Inducible no synthase gene expression was assessed by reverse-transcriptase polymerase chain reaction (RT-PCR). Colitis animals showed elevations of plasma and urine levels of reactive nitrogen intermediates of 13 and 5 fold respectively, over controls. Nadph diaphorase activity was limited to the myenteric plexus in normal controls, while colitis animals showed reactivity in crypt abscesses, superficial epithelium and mucosal bands. Gene expression for inducible no synthase was found only in colitis specimens. These observations of increased no production, inducible no synthase activity and gene expression, and localization of no synthesis to sites of injury is consistent with the hypothesis that excess no contributes to the mucosal inflammation and clinical signs of this idiopathic colitis model system.

一氧化氮（NO）在慢性特发性肾病发病机制中的作用 在幼年恒河猴中评估结肠炎。 场地、酶 在幼年恒河猴中确定了不产生的来源和程度 诊断患有慢性结肠炎/腹泻，并计划安乐死。 没有根据血浆和尿液水平对产量进行系统评估 活性氮中间体，并通过 NADPH 局部在结肠中 心肌黄酶组织化学。诱导无合酶基因表达 通过逆转录酶聚合酶链反应（RT-PCR）进行评估。 结肠炎动物的血浆和尿液反应性水平升高 氮中间体分别是对照的 13 倍和 5 倍。 正常情况下，Nadph 黄酶活性仅限于肌间神经丛。 对照组，而结肠炎动物在隐窝脓肿中表现出反应性， 浅表上皮和粘膜带。 诱导型基因表达 仅在结肠炎标本中未发现合酶。这些观察 增加无产量、诱导无合酶活性和基因 表达，并且不合成到损伤部位的定位是 与过量的 no 有助于粘膜的假设相一致 该特发性结肠炎模型系统的炎症和临床症状。