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本文引用的文献

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The action of mucin in promoting infections: the anticomplementary effect of mucin extracts and certain other substances.黏蛋白在促进感染中的作用:黏蛋白提取物及某些其他物质的抗补体效应。
Br J Exp Pathol. 1952 Aug;33(4):327-39.
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INHIBITION OF COMPLEMENT BY CARRAGEENIN: MODE OF ACTION, EFFECT ON ALLERGIC REACTIONS AND ON COMPLEMENT OF VARIOUS SPECIES.角叉菜胶对补体的抑制作用:作用方式、对过敏反应及不同物种补体的影响
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THE INTERACTION BETWEEN CARRAGEENAN AND THE FIRST COMPONENT OF COMPLEMENT.角叉菜胶与补体第一成分之间的相互作用
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5-Hydroxytryptamine and the anaphylactoid reaction in the rat.5-羟色胺与大鼠类过敏反应
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Synthetic modulators of the complement system. 1. Synthesis and biological activity of 5,5',5''-[1,3,6-naphthalenetriyltris(sulfonylimino)]-tris[1,3-benzenedisulfonic acid] hexasodium salt.补体系统的合成调节剂。1. 5,5',5''-[1,3,6-萘三基三(磺酰亚氨基)]-三[1,3-苯二磺酸]六钠盐的合成与生物活性
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Complement in acute inflammation.急性炎症中的补体
J Pathol. 1969 Feb;97(2):295-305. doi: 10.1002/path.1710970215.
9
Anti-inflammatory properties of sulfated polysaccharides and activation of the plasma kinin-forming systems.硫酸化多糖的抗炎特性及血浆激肽形成系统的激活。
Arch Int Pharmacodyn Ther. 1972 Jan;195(1):33-51.
10
Biological properties of carrageenan.卡拉胶的生物学特性。
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氯唑坚牢红2BL的补体抑制和抗炎特性

Complement-inhibiting and anti-inflammatory properties of chlorazole fast pink 2BL.

作者信息

Doherty N S

出版信息

Clin Exp Immunol. 1981 Feb;43(2):260-9.

PMID:7273480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1537288/
Abstract

Chlorazole fast pink 2BL inhibited the classical complement pathway in rat serum both in vivo and in vitro. The in vitro potency of chlorazole fast pink against the alternative pathway could not be assessed accurately but it was clearly less than that against the classical pathway. The compound appears to bind strongly to albumin with a resulting decrease in potency in undiluted as compared to diluted serum. Anti-inflammatory activity was observed in models of inflammation known to be highly complement-dependent (direct passive Arthus, zymosan oedema) but not in models in which complement is not involved (dextran oedema) or plays a minor role (carrageenan oedema).

摘要

氯唑坚牢红2BL在体内和体外均能抑制大鼠血清中的经典补体途径。氯唑坚牢红对替代途径的体外效力无法准确评估,但明显低于其对经典途径的效力。该化合物似乎与白蛋白紧密结合,导致与稀释血清相比,在未稀释血清中的效力降低。在已知高度依赖补体的炎症模型(直接被动Arthus反应、酵母聚糖水肿)中观察到抗炎活性,但在补体不参与(右旋糖酐水肿)或起次要作用(角叉菜胶水肿)的模型中未观察到。