Lanreotide protects against LPS-induced inflammation in endothelial cells and mouse lungs.

IF 4 Q2 MEDICINE, RESEARCH & EXPERIMENTAL

Tissue Barriers Pub Date : 2025-04-17 DOI:10.1080/21688370.2025.2493968

Md Matiur Rahman Sarker, Saikat Fakir, Khadeja-Tul Kubra, Madan Sigdel, Agnieszka Siejka, Henryk Stepien, Nektarios Barabutis

{"title":"Lanreotide protects against LPS-induced inflammation in endothelial cells and mouse lungs.","authors":"Md Matiur Rahman Sarker, Saikat Fakir, Khadeja-Tul Kubra, Madan Sigdel, Agnieszka Siejka, Henryk Stepien, Nektarios Barabutis","doi":"10.1080/21688370.2025.2493968","DOIUrl":null,"url":null,"abstract":"<p><p>Somatostatin is expressed in various tissues - including the hypothalamus - and strongly suppresses Growth Hormone levels to maintain homeostasis. Synthetic somatostatin analogs are currently used in clinics to treat neuroendocrine tumors and acromegaly. An emerging body of evidence suggests that those synthetic peptides exert anti-inflammatory activities. The present study examines the effect of Lanreotide (LAN) on Lipopolysaccharide (LPS)-triggered injury in endothelial cells and mice. Our findings indicate that LAN effectively mitigates LPS-induced endothelial hyperpermeability, inflammation, and reactive oxygen species (ROS) generation in bovine pulmonary artery endothelial cells (BPAEC) and human lung microvascular endothelial cells (HULEC-5a). A murine model of LPS-induced acute lung injury was also utilized, to examine the effects of LAN in lung edema and inflammation. Our observations suggest that LAN suppresses LPS-induced myosin light chain 2 (MLC2), Cofilin, extracellular signal-regulated kinase 1/2 (ERK1/2), STAT1, STAT3, P38 activation; and lung edema. In conclusion, and based on the aforementioned observations, it is suggested that LAN counteracts experimental LPS-induced injury in endothelial cells and mice.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2493968"},"PeriodicalIF":4.0000,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue Barriers","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/21688370.2025.2493968","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}

引用次数: 0

Abstract

Somatostatin is expressed in various tissues - including the hypothalamus - and strongly suppresses Growth Hormone levels to maintain homeostasis. Synthetic somatostatin analogs are currently used in clinics to treat neuroendocrine tumors and acromegaly. An emerging body of evidence suggests that those synthetic peptides exert anti-inflammatory activities. The present study examines the effect of Lanreotide (LAN) on Lipopolysaccharide (LPS)-triggered injury in endothelial cells and mice. Our findings indicate that LAN effectively mitigates LPS-induced endothelial hyperpermeability, inflammation, and reactive oxygen species (ROS) generation in bovine pulmonary artery endothelial cells (BPAEC) and human lung microvascular endothelial cells (HULEC-5a). A murine model of LPS-induced acute lung injury was also utilized, to examine the effects of LAN in lung edema and inflammation. Our observations suggest that LAN suppresses LPS-induced myosin light chain 2 (MLC2), Cofilin, extracellular signal-regulated kinase 1/2 (ERK1/2), STAT1, STAT3, P38 activation; and lung edema. In conclusion, and based on the aforementioned observations, it is suggested that LAN counteracts experimental LPS-induced injury in endothelial cells and mice.

查看原文本刊更多论文

Lanreotide对lps诱导的内皮细胞和小鼠肺炎症具有保护作用。

生长抑素在包括下丘脑在内的各种组织中表达，并强烈抑制生长激素水平以维持体内平衡。合成生长抑素类似物目前用于临床治疗神经内分泌肿瘤和肢端肥大症。越来越多的证据表明，这些合成肽具有抗炎作用。本研究探讨了Lanreotide （LAN）对脂多糖（LPS）引发的内皮细胞和小鼠损伤的影响。我们的研究结果表明，LAN可以有效减轻lps诱导的牛肺动脉内皮细胞（BPAEC）和人肺微血管内皮细胞（HULEC-5a）内皮细胞的高通透性、炎症和活性氧（ROS）的产生。采用lps致小鼠急性肺损伤模型，观察LAN对肺水肿和炎症的影响。我们的观察结果表明，LAN抑制lps诱导的肌球蛋白轻链2 （MLC2）、Cofilin、细胞外信号调节激酶1/2 （ERK1/2）、STAT1、STAT3、P38的激活；还有肺水肿。综上所述，基于上述观察结果，我们认为LAN可以抵消实验性lps诱导的内皮细胞和小鼠损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Tissue Barriers MEDICINE, RESEARCH & EXPERIMENTAL-

CiteScore

6.60

自引率

6.50%

发文量

期刊介绍： Tissue Barriers is the first international interdisciplinary journal that focuses on the architecture, biological roles and regulation of tissue barriers and intercellular junctions. We publish high quality peer-reviewed articles that cover a wide range of topics including structure and functions of the diverse and complex tissue barriers that occur across tissue and cell types, including the molecular composition and dynamics of polarized cell junctions and cell-cell interactions during normal homeostasis, injury and disease state. Tissue barrier formation in regenerative medicine and restoration of tissue and organ function is also of interest. Tissue Barriers publishes several categories of articles including: Original Research Papers, Short Communications, Technical Papers, Reviews, Perspectives and Commentaries, Hypothesis and Meeting Reports. Reviews and Perspectives/Commentaries will typically be invited. We also anticipate to publish special issues that are devoted to rapidly developing or controversial areas of research. Suggestions for topics are welcome. Tissue Barriers objectives: Promote interdisciplinary awareness and collaboration between researchers working with epithelial, epidermal and endothelial barriers and to build a broad and cohesive worldwide community of scientists interesting in this exciting field. Comprehend the enormous complexity of tissue barriers and map cross-talks and interactions between their different cellular and non-cellular components. Highlight the roles of tissue barrier dysfunctions in human diseases. Promote understanding and strategies for restoration of tissue barrier formation and function in regenerative medicine. Accelerate a search for pharmacological enhancers of tissue barriers as potential therapeutic agents. Understand and optimize drug delivery across epithelial and endothelial barriers.