Yin Jia, Chi Yawen, Liu Danyan, Li Xinghua, Li Xu
Department of Critical Care Medicine, The First Affiliated Hospital, China Medical University, North Nanjing Street 155, Shenyang, Liaoning, 110001, China.
J Inflamm (Lond). 2025 Feb 17;22(1):9. doi: 10.1186/s12950-025-00437-x.
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).
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.
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.
UFH may attenuate histone-induced lung injury and pulmonary endothelial glycocalyx degradation via the Ang/Tie2 pathway.
本研究旨在探讨血管生成素（Ang）/Tie2通路在介导组蛋白诱导的小鼠急性肺损伤中肺内皮糖萼损伤的作用，以及普通肝素（UFH）的保护机制。
将24只8 - 12周龄、体重20 - 25 g的雄性C57BL/6小鼠随机分为对照组、组蛋白组和组蛋白+UFH组。通过尾静脉注射组蛋白（50 mg/kg）。在注射组蛋白1小时后给予UFH（400 U/kg）。对照组给予等量的无菌生理盐水溶液。在注射组蛋白或无菌生理盐水4小时后，采集所有组小鼠的肺组织。
UFH减轻了组蛋白诱导的肺组织病理变化和水肿。UFH通过减少组蛋白诱导的血栓调节蛋白（TM）低表达和降低肺组织中syndecan-1水平，减轻了肺内皮损伤和糖萼脱落。UFH改善了组蛋白诱导的TM、syndecan-1、Ang-1、Tie2 mRNA低表达以及肝素酶（HPA）、Ang-2高表达。
UFH可能通过Ang/Tie2通路减轻组蛋白诱导的肺损伤和肺内皮糖萼降解。
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