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2
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本文引用的文献

1
Ultraweak chemiluminescence: a sensitive assay for oxidative radical reactions.超微弱化学发光:一种用于氧化自由基反应的灵敏检测方法。
Fed Proc. 1981 Feb;40(2):195-8.
2
Recent developments in "nonspecific" inflammatory bowel disease (first of two parts).“非特异性”炎症性肠病的最新进展(第一部分)
N Engl J Med. 1982 Apr 1;306(13):775-85. doi: 10.1056/NEJM198204013061304.
3
Organ chemiluminescence: noninvasive assay for oxidative radical reactions.有机化学发光:氧化自由基反应的非侵入性检测方法。
Proc Natl Acad Sci U S A. 1980 Jan;77(1):347-51. doi: 10.1073/pnas.77.1.347.
4
Role of oxygen-derived free radicals in digestive tract diseases.氧衍生自由基在消化道疾病中的作用。
Surgery. 1983 Sep;94(3):415-22.
5
Ischemia-induced vascular changes: role of xanthine oxidase and hydroxyl radicals.缺血诱导的血管变化:黄嘌呤氧化酶和羟自由基的作用
Am J Physiol. 1983 Aug;245(2):G285-9. doi: 10.1152/ajpgi.1983.245.2.G285.
6
Role of myeloperoxidase in luminol-dependent chemiluminescence of polymorphonuclear leukocytes.髓过氧化物酶在多形核白细胞鲁米诺依赖性化学发光中的作用
Infect Immun. 1983 Feb;39(2):736-41. doi: 10.1128/iai.39.2.736-741.1983.
7
Mechanism of the luminol-dependent chemiluminescence of human neutrophils.人中性粒细胞鲁米诺依赖性化学发光的机制
J Immunol. 1982 Oct;129(4):1589-93.
8
Relapse of ulcerative proctocolitis during treatment with non-steroidal anti-inflammatory drugs.非甾体抗炎药治疗期间溃疡性直肠结肠炎的复发
Postgrad Med J. 1981 May;57(667):297-9. doi: 10.1136/pgmj.57.667.297.
9
Prostaglandin synthesis inhibitors in ulcerative colitis: flurbiprofen compared with conventional treatment.溃疡性结肠炎中的前列腺素合成抑制剂:氟比洛芬与传统治疗的比较
Prostaglandins. 1981 Mar;21(3):417-25. doi: 10.1016/0090-6980(81)90087-3.
10
Quantitative assay for acute intestinal inflammation based on myeloperoxidase activity. Assessment of inflammation in rat and hamster models.基于髓过氧化物酶活性的急性肠道炎症定量测定。大鼠和仓鼠模型炎症评估。
Gastroenterology. 1984 Dec;87(6):1344-50.

溃疡性结肠炎患者发炎的结肠黏膜增加了鲁米诺的产生,从而增强了化学发光。

Increased production of luminol enhanced chemiluminescence by the inflamed colonic mucosa in patients with ulcerative colitis.

作者信息

Sedghi S, Fields J Z, Klamut M, Urban G, Durkin M, Winship D, Fretland D, Olyaee M, Keshavarzian A

机构信息

Department of Medicine, Loyola University Medical Center, Maywood, IL 60153.

出版信息

Gut. 1993 Sep;34(9):1191-7. doi: 10.1136/gut.34.9.1191.

DOI:10.1136/gut.34.9.1191
PMID:8406152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1375452/
Abstract

Reactive oxygen species have been implicated as mediators of inflammation in ulcerative colitis. Chemiluminescence is a reliable means of estimating reactive oxygen species in biological media. Increased reactive oxygen species values in the inflamed colonic mucosa in rats were seen by chemiluminescence. The aims of the study were to find out if chemiluminescence is raised in the colonic mucosa of patients with ulcerative colitis and correlates with disease activity, and to elucidate the sources of the chemiluminescence. It was found that reactive oxygen species, as measured by the chemiluminescence technique, are raised in inflamed colonic mucosa and correlates with symptom score, sigmoidoscopic score, disease activity, and activity of the neutrophil enzyme myeloperoxidase. Chemiluminescence was inhibited by a myeloperoxidase inhibitor (azide) and an H2O2 scavenger (catalase) but not by allopurinol, an inhibitor of the enzyme xanthine oxidase. Chemiluminescence was also inhibited by indomethacin, but this did not seem to be related to inhibition of cyclo-oxygenase. These findings suggest that a likely cellular source of reactive oxygen species in the inflamed colon of patients with ulcerative colitis is the neutrophil and that myeloperoxidase conversion of H2O2 to hypochlorous acid, contributes to the chemiluminescence signal and possibly, to the tissue injury. Neither cyclo-oxygenase nor lipoxygenase seem to play a part as sources for the chemiluminescence.

摘要

活性氧被认为是溃疡性结肠炎炎症的介质。化学发光是评估生物介质中活性氧的可靠方法。通过化学发光观察到大鼠炎症性结肠黏膜中的活性氧值升高。本研究的目的是确定溃疡性结肠炎患者的结肠黏膜中化学发光是否升高并与疾病活动相关,以及阐明化学发光的来源。结果发现,通过化学发光技术测量的活性氧在炎症性结肠黏膜中升高,并与症状评分、乙状结肠镜评分、疾病活动度以及中性粒细胞酶髓过氧化物酶的活性相关。化学发光被髓过氧化物酶抑制剂(叠氮化物)和H2O2清除剂(过氧化氢酶)抑制,但不被黄嘌呤氧化酶抑制剂别嘌呤醇抑制。消炎痛也抑制化学发光,但这似乎与环氧化酶的抑制无关。这些发现表明,溃疡性结肠炎患者炎症结肠中活性氧的可能细胞来源是中性粒细胞,并且髓过氧化物酶将H2O2转化为次氯酸,有助于化学发光信号,并可能导致组织损伤。环氧化酶和脂氧合酶似乎都不是化学发光的来源。