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抗血浆渗漏的潜在药物。

Potential Agents against Plasma Leakage.

作者信息

Pawitan Jeanne Adiwinata

机构信息

Department of Histology, Faculty of Medicine, University of Indonesia, Jl. Salemba 6, Jakarta 10430, Indonesia.

出版信息

ISRN Pharmacol. 2011;2011:975048. doi: 10.5402/2011/975048. Epub 2011 Apr 3.

DOI:10.5402/2011/975048
PMID:22084722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3195382/
Abstract

Shock due to severe plasma leakage may happen in infectious diseases such as severe dengue and sepsis due to various bacterial infections, which may be deleterious and may lead to death. Various substances and proteins are known to modulate the effects of proleakage mediators and counteract the deleterious effect of plasma leakage. Some of the various substances and proteins such as focal adhesion kinase (FAK), the Rho GTPases, protein kinase A, and caveolin-1 have dual actions; therefore they are not suitable for therapy. However, sphingosine 1phosphate and its receptor agonists, Angiopoetin-1, Slit, and Bbeta15-42 may be promising.

摘要

严重血浆渗漏导致的休克可能发生在诸如严重登革热等传染病以及各种细菌感染引起的败血症中，这可能是有害的，甚至可能导致死亡。已知多种物质和蛋白质可调节促渗漏介质的作用，并抵消血浆渗漏的有害影响。多种物质和蛋白质中的一些，如粘着斑激酶（FAK）、Rho GTP酶、蛋白激酶A和小窝蛋白-1具有双重作用；因此它们不适合用于治疗。然而，1-磷酸鞘氨醇及其受体激动剂、血管生成素-1、Slit和β淀粉样蛋白15-42可能很有前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/89ab15e265d7/PHARMACOLOGY2011-975048.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/ae96f87f7836/PHARMACOLOGY2011-975048.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/702cf0cb95ab/PHARMACOLOGY2011-975048.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/6297b97c7c8b/PHARMACOLOGY2011-975048.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/89ab15e265d7/PHARMACOLOGY2011-975048.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/ae96f87f7836/PHARMACOLOGY2011-975048.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/702cf0cb95ab/PHARMACOLOGY2011-975048.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/6297b97c7c8b/PHARMACOLOGY2011-975048.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9eb/3195382/89ab15e265d7/PHARMACOLOGY2011-975048.004.jpg

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本文引用的文献

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Sepsis and endothelial permeability.脓毒症与内皮通透性。
N Engl J Med. 2010 Aug 12;363(7):689-91. doi: 10.1056/NEJMcibr1007320.
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Targeting Robo4-dependent Slit signaling to survive the cytokine storm in sepsis and influenza.针对 Robo4 依赖性 Slit 信号转导以在脓毒症和流感的细胞因子风暴中存活。
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Caveolin-1 regulates VEGF-stimulated angiogenic activities in prostate cancer and endothelial cells.窖蛋白-1 调节前列腺癌和内皮细胞中血管内皮生长因子刺激的血管生成活性。
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Slit2-Robo4 signalling promotes vascular stability by blocking Arf6 activity.Slit2-Robo4信号通路通过阻断Arf6活性来促进血管稳定性。
Nat Cell Biol. 2009 Nov;11(11):1325-31. doi: 10.1038/ncb1976. Epub 2009 Oct 18.
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FX-06, a fibrin-derived Bbeta15-42 peptide for the potential treatment of reperfusion injury following myocardial infarction.FX-06，一种源自纤维蛋白的Bβ15-42肽，用于心肌梗死后再灌注损伤的潜在治疗。
Curr Opin Investig Drugs. 2009 Sep;10(9):997-1003.
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Sphingosine-1-phosphate in the plasma compartment regulates basal and inflammation-induced vascular leak in mice.血浆中的1-磷酸鞘氨醇调节小鼠的基础血管渗漏和炎症诱导的血管渗漏。
J Clin Invest. 2009 Jul;119(7):1871-9. doi: 10.1172/jci38575.
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