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本文引用的文献

1
Immunologic and neuropharmacologic stimulation of mucous glycoprotein release from human airways in vitro.体外对人呼吸道黏液糖蛋白释放的免疫和神经药理学刺激。
J Clin Invest. 1980 Dec;66(6):1400-8. doi: 10.1172/JCI109993.
2
Effects of arachidonic acid, monohydroxyeicosatetraenoic acid and prostaglandins on the release of mucous glycoproteins from human airways in vitro.花生四烯酸、单羟基二十碳四烯酸和前列腺素对人气道黏液糖蛋白体外释放的影响。
J Clin Invest. 1981 Jun;67(6):1695-702. doi: 10.1172/jci110207.
3
The effects of corticosteroids on mucous glycoprotein secretion from human airways in vitro.皮质类固醇对人呼吸道黏液糖蛋白体外分泌的影响。
Am Rev Respir Dis. 1984 Jan;129(1):62-5. doi: 10.1164/arrd.1984.129.1.62.
4
Predominant generation of 15-lipoxygenase metabolites of arachidonic acid by epithelial cells from human trachea.人气管上皮细胞主要生成花生四烯酸的15-脂氧合酶代谢产物。
Proc Natl Acad Sci U S A. 1985 Jul;82(14):4633-7. doi: 10.1073/pnas.82.14.4633.
5
15-Hydroxyeicosatetraenoic acid is a potent inflammatory mediator and agonist of canine tracheal mucus secretion.
Am Rev Respir Dis. 1985 Jun;131(6):917-22. doi: 10.1164/arrd.1985.131.6.917.
6
Monoclonal antibodies against oncofetal mucin M1 antigens associated with precancerous colonic mucosae.针对与癌前结肠黏膜相关的癌胚黏蛋白M1抗原的单克隆抗体。
Cancer Res. 1986 Aug;46(8):3983-9.
7
Airway smooth muscle and disease workshop: histamine and prostanoids.气道平滑肌与疾病研讨会:组胺和前列腺素
Am Rev Respir Dis. 1987 Oct;136(4 Pt 2):S21-4. doi: 10.1164/ajrccm/136.4_Pt_2.S21.
8
The detection of 5-lipoxygenase and cyclo-oxygenase products in sputum of patients with chronic bronchitis and bronchiectasis.慢性支气管炎和支气管扩张症患者痰液中5-脂氧合酶和环氧化酶产物的检测
Prostaglandins. 1987 May;33(5):663-74. doi: 10.1016/0090-6980(87)90033-5.
9
Chemical properties of bronchorrhea sputum in bronchial asthma.
Chest. 1988 Dec;94(6):1211-5. doi: 10.1378/chest.94.6.1211.
10
Lipid mediators in cystic fibrosis and chronic obstructive pulmonary disease.囊性纤维化和慢性阻塞性肺疾病中的脂质介质。
Am Rev Respir Dis. 1987 Sep;136(3):779-82. doi: 10.1164/ajrccm/136.3.779.

吲哚美辛和Bay X1005对人呼吸道体外释放MUC5AC黏蛋白的影响

MUC5AC mucin release from human airways in vitro: effects of indomethacin and Bay X1005.

作者信息

Roger P, Gascard J P, Bara J, de Montpreville V T, Brink C

机构信息

Laboratoire de Pharmacologie Pulmonaire, CNRS-ESA 8078, H pital Marie Lannelongue, Le Plessis Robinson, France.

出版信息

Mediators Inflamm. 2001 Feb;10(1):33-6. doi: 10.1080/09629350124329.

DOI:10.1080/09629350124329
PMID:11324902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1781691/
Abstract

BACKGROUND

Increased secretion of mucus is a hallmark of many respiratory diseases and contributes significantly to the airflow limitation experienced by many patients. While the current pharmacological approach to reducing mucus and sputum production in patients is limited, clinical studies have suggested that drugs which inhibit the cyclooxygenase and/or 5-lipoxygenase enzymatic pathways may reduce secretory activity in patients with airway disease.

AIM

This study was performed to investigate the effects of indomethacin (cyclooxygenase inhibitor) and Bay x 1005 (5-lipoxygenase inhibitor) on MUC5AC release from human airways in vitro.

METHODS

An immunoradiometric assay was used to determine the quantities of MUC5AC present in the biological fluids derived from human airways in vitro. The measurements were made with a mixture of eight monoclonal antibodies (MAbs; PM8) of which the 21 M1 MAb recognized a recombinant M1 mucin partially encoded by the MUC5AC gene.

RESULTS

The quantities of MUC5AC detected in the biological fluids derived from human bronchial preparations were not modified after treatment with indomethacin (cyclooxygenase inhibitor) and/or an inhibitor of the 5-lipoxygenase metabolic pathway (BAY x 1005).

CONCLUSION

These results suggest that the cyclooxygenase and 5-lipoxygenase metabolic pathways play little or no role in the release of MUC5AC from human airways.

摘要

背景

黏液分泌增加是许多呼吸道疾病的一个标志,并且是导致许多患者气流受限的重要因素。虽然目前用于减少患者黏液和痰液生成的药理学方法有限,但临床研究表明,抑制环氧化酶和/或5-脂氧合酶酶促途径的药物可能会降低气道疾病患者的分泌活性。

目的

本研究旨在调查吲哚美辛(环氧化酶抑制剂)和Bay x 1005(5-脂氧合酶抑制剂)对体外人气道MUC5AC释放的影响。

方法

采用免疫放射分析法定量测定体外人气道生物流体中MUC5AC的含量。测量使用了八种单克隆抗体(MAb;PM8)的混合物,其中21 M1 MAb识别由MUC5AC基因部分编码的重组M1黏蛋白。

结果

用吲哚美辛(环氧化酶抑制剂)和/或5-脂氧合酶代谢途径抑制剂(BAY x 1005)处理后,人支气管制剂生物流体中检测到的MUC5AC含量未发生改变。

结论

这些结果表明,环氧化酶和5-脂氧合酶代谢途径在人气道MUC5AC释放中作用很小或没有作用。