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1-哌啶丙酸通过蛋白酶受体 2 抑制保护脓毒性休克。

1-Piperidine Propionic Acid Protects from Septic Shock Through Protease Receptor 2 Inhibition.

机构信息

Department of Surgical, Oncological and Gastroenterological Sciences, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.

Department of Medicine, Azienda Ospedaliera-Università Padova, Via Giustiniani 2, 35128 Padova, Italy.

出版信息

Int J Mol Sci. 2024 Oct 30;25(21):11662. doi: 10.3390/ijms252111662.

DOI:10.3390/ijms252111662
PMID:39519216
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11547144/
Abstract

Sepsis is a complex disorder caused by a dysregulated host response to infection, with high levels of morbidity and mortality. Treatment aimed to modulate immune response and maintain vascular function is still one of the major clinical challenges. This study was designed to test the effect of the small molecule 1-Piperidine Propionic Acid (1-PPA) as molecular targeted agent to block protease-activated receptor 2 (PAR2), one of the major modulators of inflammatory response in LPS-induced experimental endotoxemia. In the THP-1 cell line, LPS-induced cytokine expression was inhibited by 1-PPA in a dose-dependent manner. In LPS-injected mice, treatment with 1-PPA was effective in reducing mortality and sepsis-related symptoms and improved cardiac function parameters. After 6 h from LPS injection, a significant decrease in IL-6, IL-1β, and IL-10 was observed in the lung tissue of 1-PPA-treated mice, compared to controls. In these mice, a significant decrease in vasoactive molecules, especially kininogen-1, was also observed, mainly in the liver. Histopathological analysis confirmed typical features of sepsis in different organs and these findings were markedly reduced in mice treated with 1-PPA. These data demonstrate the effectiveness of 1-PPA in protecting the whole organism from sepsis-induced damage.

摘要

脓毒症是一种由宿主对感染的失调反应引起的复杂疾病,具有高发病率和死亡率。旨在调节免疫反应和维持血管功能的治疗仍然是主要的临床挑战之一。本研究旨在测试小分子 1-哌啶丙酸(1-PPA)作为分子靶向剂的效果,以阻断蛋白酶激活受体 2(PAR2),这是 LPS 诱导的实验性内毒素血症中炎症反应的主要调节剂之一。在 THP-1 细胞系中,LPS 诱导的细胞因子表达被 1-PPA 以剂量依赖性方式抑制。在 LPS 注射的小鼠中,用 1-PPA 治疗可有效降低死亡率和与脓毒症相关的症状,并改善心脏功能参数。与对照组相比,在 LPS 注射后 6 小时,1-PPA 治疗的小鼠肺组织中的 IL-6、IL-1β 和 IL-10 显著减少。在这些小鼠中,还观察到血管活性分子,特别是激肽原-1 的显著减少,主要在肝脏中。组织病理学分析证实了不同器官中脓毒症的典型特征,而用 1-PPA 治疗的小鼠中这些发现明显减少。这些数据表明 1-PPA 可有效保护整个机体免受脓毒症引起的损伤。

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