Unfractionated heparin attenuated histone-induced pulmonary endothelial glycocalyx injury through Ang/Tie2 pathway.

IF 4.4 3区医学 Q2 IMMUNOLOGY

Journal of Inflammation-London Pub Date : 2025-02-17 DOI:10.1186/s12950-025-00437-x

Jia Yin, Yawen Chi, Danyan Liu, Xinghua Li, Xu Li

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引用次数: 0

Abstract

Purpose: This study aimed to investigate the involvement of angiopoietin (Ang)/Tie2 pathway in mediating pulmonary endothelial glycocalyx injury in histone-induced acute lung injury in mice, and the protective mechanism of unfractionated heparin (UFH).

Methods: Twenty-four male C57BL/6 mice (20-25 g), 8-12 weeks old, were randomly divided into control, histone, and histone + UFH groups. The histone (50 mg/kg) was administered via tail vein. UFH (400 U/kg) was administered 1 h after histone injection. The control group was administered by an equal amount of sterile saline solution. The lungs of all groups were harvested 4 h after the injection of histones or sterile saline.

Results: UFH attenuated histone-induced lung histopathological changes and edema. UFH alleviated pulmonary endothelial injury and glycocalyx shedding by reducing histone-induced low expression of thrombomodulin (TM) and decreased lung syndecan-1 levels. UFH improved histone-induced low mRNA expression of TM, syndecan-1, Ang-1, Tie2 and high expression of heparinase (HPA), Ang-2.

Conclusion: UFH may attenuate histone-induced lung injury and pulmonary endothelial glycocalyx degradation via the Ang/Tie2 pathway.

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未分离肝素通过Ang/Tie2途径减轻组蛋白诱导的肺内皮糖萼损伤。

目的：本研究旨在探讨血管生成素(angiopoietin, Ang)/Tie2通路在组蛋白诱导的小鼠急性肺损伤中介导肺内皮糖盏损伤的作用，以及未分离肝素（uhf）的保护机制。方法：8 ~ 12周龄雄性C57BL/6小鼠24只（20 ~ 25 g），随机分为对照组、组蛋白组和组蛋白+ UFH组。组蛋白（50 mg/kg）经尾静脉给药。组蛋白注射后1 h给药UFH （400u /kg）。对照组给予等量无菌生理盐水溶液。各组在注射组蛋白或无菌生理盐水4 h后取肺。结果：UFH可减轻组蛋白引起的肺组织病理改变和水肿。UFH通过降低组蛋白诱导的血栓调节素（TM）低表达和肺syndecan-1水平，减轻肺内皮损伤和糖环脱落。UFH改善了组蛋白诱导的TM、syndecan-1、Ang-1、Tie2 mRNA的低表达和肝素酶（HPA）、Ang-2 mRNA的高表达。结论：UFH可通过Ang/Tie2途径减轻组蛋白诱导的肺损伤和肺内皮糖萼降解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Inflammation-London IMMUNOLOGY-

CiteScore

7.90

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.