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首页> 外文期刊>Cellular Physiology and Biochemistry >Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions
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Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions

机译：尿胰蛋白酶抑制剂通过改善内皮祖细胞功能减轻急性肺损伤。

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Background: Urinary Trypsin Inhibitor (UTI) is involved in various aspects of tissue repair, regeneration and development. However, the potential role of UTI in protection against acute lung injury (ALI) remains largely unknown. In the present study, we demonstrated that UTI treatment could ameliorate ALI induced by oleic acid (OA) treatment in rabbit model. Methods: Intravenous application of UTI (10000 U/kg/d) significantly improved the pathologies associated with OA-induced ALI. The lungs were stained with hematoxylin and eosin to scored the lung injury. Peripheral blood mononuclear cells were isolated by density gradient centrifugation with Ficoll-Plaque Plus. The proliferation and ability of tube structure formation of EPCs were observed and the level of phosphorylated Akt protein expression and eNOS protein expression were assayed. Results: Consistent with pathological scores, UTI treatment significantly reduced wet/dry ratio of OA injured lungs. A quantification of capillary density revealed that UTI treatment led to about 2 fold increase over uninjured control and about 1.5 fold increase over PBS treatment. The capacity for tube formation of EPCs on ECM gel was significantly reduced in the ALI group and recovered with UTI treatment. Quantification of western blot bands was summarized and showed that UTI treatment activates Akt/eNOS signaling. NO production could contribute to the improvement of EPCs function by UTI treatment. Conclusions: UTI-induced phosphorylation/activation of eNOS and Akt, increases the intracellular level of NO, thereby improving tube formation and proliferation function of EPCs. EPCs function is crucial for re-endothelialization after denuding injuries of arteries.
机译：背景：尿胰蛋白酶抑制剂（UTI）涉及组织修复，再生和发育的各个方面。但是，UTI在预防急性肺损伤（ALI）方面的潜在作用仍然未知。在本研究中，我们证明了UTI治疗可以改善兔模型中油酸（OA）处理诱导的ALI。方法：静脉滴注尿路感染（10000 U / kg / d）可显着改善与OA诱导的ALI相关的病理。用苏木精和曙红对肺部进行染色以评分肺部损伤。通过用Ficoll-Plaque Plus进行密度梯度离心来分离外周血单个核细胞。观察EPCs的增殖和管结构形成能力，并测定磷酸化的Akt蛋白表达和eNOS蛋白表达水平。结果：与病理学评分一致，UTI治疗显着降低了OA损伤的肺的干/湿比。毛细血管密度的定量显示，UTI处理比未受伤的对照增加了约2倍，而PBS处理增加了约1.5倍。 ALI组在ECM凝胶上形成EPC的管的能力显着降低，并通过UTI处理得以恢复。总结了蛋白质印迹带的定量，并显示了UTI处理可激活Akt / eNOS信号传导。没有生产可以通过UTI处理促进EPC功能的改善。结论：UTI诱导eNOS和Akt的磷酸化/激活，增加了细胞内NO的水平，从而改善了EPC的管形成和增殖功能。 EPCs功能在剥夺动脉损伤后对于重新内皮化至关重要。

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