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炎症会引发小鼠体内的低铁血症以及血清转铁蛋白和铜蓝蛋白的从头合成。

Inflammation triggers hypoferremia and de novo synthesis of serum transferrin and ceruloplasmin in mice.

作者信息

Beaumier D L, Caldwell M A, Holbein B E

出版信息

Infect Immun. 1984 Nov;46(2):489-94. doi: 10.1128/iai.46.2.489-494.1984.

Abstract

Oil of turpentine was used to induce an artificial inflammation so that we could study its effect on iron metabolism and on synthesis of serum transferrin and ceruloplasmin in mice. It was found that turpentine-induced inflammation triggered the establishment of a hypoferremic state characterized by low levels of serum iron, followed by recovery and a gradual return to normal plasma iron levels. This turpentine-induced hypoferremia and its subsequent recovery paralleled the hypoferremia obtained during meningococcal infection. Moreover, serum transferrin and ceruloplasmin activity levels increased drastically during the recovery from hypoferremia. [14C]leucine incorporation studies revealed a de novo synthesis of both transferrin and ceruloplasmin. Turpentine-induced hypoferremia was also found to provide a protective effect against meningococcal infection which could be partially reversed by exogenous iron. The results of this study suggest that transferrin and ceruloplasmin may be synthesized partly in response to the altered iron metabolism observed during hypoferremia.

摘要

松节油被用于诱发人工炎症,以便我们能够研究其对小鼠铁代谢以及血清转铁蛋白和铜蓝蛋白合成的影响。结果发现,松节油诱发的炎症引发了低铁血症状态的建立,其特征为血清铁水平降低,随后恢复并逐渐回到正常血浆铁水平。这种松节油诱发的低铁血症及其随后的恢复与脑膜炎球菌感染期间出现的低铁血症相似。此外,在从低铁血症恢复过程中,血清转铁蛋白和铜蓝蛋白活性水平急剧增加。[14C]亮氨酸掺入研究显示转铁蛋白和铜蓝蛋白均有从头合成。还发现松节油诱发的低铁血症对脑膜炎球菌感染具有保护作用,而外源性铁可部分逆转这种作用。本研究结果表明,转铁蛋白和铜蓝蛋白的合成可能部分是对低铁血症期间观察到的铁代谢改变作出的反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2f2/261560/84802c2f2b22/iai00122-0211-a.jpg

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