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一种新型小分子TLR4拮抗剂(IAXO-102)对非造血性Toll样受体4信号传导起负调节作用,并抑制主动脉瘤的发展。

A novel small molecule TLR4 antagonist (IAXO-102) negatively regulates non-hematopoietic toll like receptor 4 signalling and inhibits aortic aneurysms development.

作者信息

Huggins Christopher, Pearce Stuart, Peri Francesco, Neumann Frank, Cockerill Gillian, Pirianov Grisha

机构信息

Institute of Cardiovascular Sciences and Cell Biology, St Georges University of London, UK.

Department of Biotechnology and Biosciences, University of Milano-Bicocca, Italy.

出版信息

Atherosclerosis. 2015 Oct;242(2):563-70. doi: 10.1016/j.atherosclerosis.2015.08.010. Epub 2015 Aug 8.

Abstract

OBJECTIVES

The toll-like receptors (TLRs), including TLR4, have been shown to play a crucial role in vascular inflammatory diseases, such as atherosclerosis and aneurysm. The main goal of this study was to determine the potential of IAXO-102 (Innaxon, Tewkesbury), a novel small molecule TLR4 antagonist, to modulate non-hematopoietic TLR4 proinflammatory signalling and inhibit experimental abdominal aortic aneurysm (AAA) development.

METHODS

Human umbilical vein endothelial cells (HUVEC) and Angiotensin II-induced experimental AAA development were our in vitro and in vivo models respectively. Western blotting, antibody array and ELISA approaches were used to explore the effect of IAXO-102 on TLR4 functional activity on two levels: modulation of TLR4-induced mitogen activated protein kinases (MAPK) and p65 NF-kB phosphorylation and expression of TLR4 dependent proinflammatory proteins.

RESULTS

Following activation of TLR4, in vitro/in vivo data revealed that IAXO-102 inhibited MAPK and p65 NF-kB phosphorylation associated with down regulation of the expression of TLR4 and TLR4 dependent proinflammatory proteins. Furthermore, IAXO-102 decreased Angiotensin II-induced aortic expansion, rupture and incidence of AAA.

CONCLUSIONS

These results demonstrate the ability of IAXO-102 to negatively regulate TLR4 signalling and to inhibit experimental AAA development, suggesting the potential therapeutic use of this TLR4 antagonist for pharmacological intervention of AAA.

摘要

目的

包括Toll样受体4(TLR4)在内的Toll样受体(TLR)已被证明在血管炎性疾病(如动脉粥样硬化和动脉瘤)中起关键作用。本研究的主要目的是确定新型小分子TLR4拮抗剂IAXO-102(Innaxon公司,图克斯伯里)调节非造血细胞TLR4促炎信号传导和抑制实验性腹主动脉瘤(AAA)发展的潜力。

方法

人脐静脉内皮细胞(HUVEC)和血管紧张素II诱导的实验性AAA发展分别作为我们的体外和体内模型。采用蛋白质印迹法、抗体芯片法和酶联免疫吸附测定法,从两个层面探讨IAXO-102对TLR4功能活性的影响:调节TLR4诱导的丝裂原活化蛋白激酶(MAPK)和p65核因子κB(NF-κB)磷酸化以及TLR4依赖性促炎蛋白的表达。

结果

激活TLR4后,体外/体内数据显示IAXO-102抑制与TLR4及TLR4依赖性促炎蛋白表达下调相关的MAPK和p65 NF-κB磷酸化。此外,IAXO-102降低了血管紧张素II诱导的主动脉扩张、破裂及AAA发生率。

结论

这些结果证明了IAXO-102负向调节TLR4信号传导并抑制实验性AAA发展的能力,提示这种TLR4拮抗剂在AAA药物干预方面具有潜在的治疗用途。

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