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锰(II)对过氧亚硝酸盐硝化纤维蛋白原的影响。

Effects of Mn (II) on peroxynitrite nitrifying fibrinogen.

作者信息

Ding Yang, Luo Yunjing, Fu Jun

机构信息

College of Life Science and Bioengineering, Beijing University of Technology, Beijing 100124, P.R. China.

出版信息

Biomed Mater Eng. 2014;24(1):901-7. doi: 10.3233/BME-130884.

Abstract

Fibrinogen is a plasma glycoprotein that is an established cardiovascular risk and it participates in the blood-clotting mechanism. Nitrated fibrinogen has been shown to inhibit platelet aggregation and thrombus formation. However, there are only a few reports relating to the activity and structural changes of nitrified fibrinogen when metal ions are present in the reaction. Mn (II) ion plays an important physiological role in the nervous system and cardiac function. In this study, we use UV-Vis, 3D-fluorescence, SDS-PAGE electrophoresis and Von-Clauss to detect 3-nitrotyrosine (3-NT) production and the activity changes of fibrinogen after nitration and oxidation damage caused by ONOO- in the presence of Mn (II). Results showed that Mn (II) can enhance the production of 3-NT in fibrinogen, promote fluorescence quenching of fibrinogen, and increase the injury to γ and Aα chains of fibrinogen in the presence of peroxynitrite. Consequently, Mn (II) promotes concentration dependent fibrinogen nitrification damage and significantly reduces the biological activity of nitrified fibrinogen.

摘要

纤维蛋白原是一种血浆糖蛋白,是一种既定的心血管风险因素,它参与血液凝固机制。已表明硝化纤维蛋白原可抑制血小板聚集和血栓形成。然而,关于反应中存在金属离子时硝化纤维蛋白原的活性和结构变化的报道较少。锰(II)离子在神经系统和心脏功能中发挥重要的生理作用。在本研究中,我们使用紫外可见光谱、三维荧光、十二烷基硫酸钠聚丙烯酰胺凝胶电泳(SDS-PAGE)和冯·克劳斯法来检测在锰(II)存在的情况下,过氧亚硝酸根(ONOO-)导致的硝化和氧化损伤后纤维蛋白原中3-硝基酪氨酸(3-NT)的产生以及纤维蛋白原的活性变化。结果表明,在过氧亚硝酸根存在的情况下,锰(II)可增强纤维蛋白原中3-NT的产生,促进纤维蛋白原的荧光猝灭,并增加对纤维蛋白原γ链和Aα链的损伤。因此,锰(II)促进浓度依赖性的纤维蛋白原硝化损伤,并显著降低硝化纤维蛋白原的生物活性。

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