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Octreotide protects against LPS-induced endothelial cell and lung injury. | LitMetric

Octreotide protects against LPS-induced endothelial cell and lung injury.

Cell Signal

School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA. Electronic address:

Published: December 2024

AI Article Synopsis

  • Growth hormone (GH) regulates growth and cell functions, controlled by GHRH and somatostatin, while LPS can damage blood vessel function and increase inflammation.
  • Octreotide (OCT), a synthetic somatostatin analog, is used for treating certain tumors and conditions like acromegaly; this study tests its effects on damage caused by LPS in lung cells.
  • Results show that OCT reduces inflammation and vascular leakage caused by LPS in bovine and human lung cells, indicating potential as a therapy for related lung injuries and diseases.

Article Abstract

Growth hormone (GH) is a crucial regulator of growth, cell reproduction, and regeneration; and it is controlled by growth hormone-releasing hormone (GHRH) and somatostatin. Lipopolysaccharides (LPS) can compromise endothelial function, leading to increased inflammation and vascular leak. Octreotide (OCT) is an FDA-approved synthetic somatostatin analog (SSA) used to treat acromegaly and neuroendocrine tumors. The present study investigates the effects of OCT on LPS-induced injury in bovine and human lung endothelial cells, as well as in mouse lungs. Our in vitro observations suggest that OCT effectively counteracts LPS-induced endothelial leak, inflammation, and reactive oxygen species (ROS) generation. Furthermore, OCT reduces bronchoalveolar lavage fluid (BALF) protein concentration in an experimental model of Acute Lung Injury (ALI). Our study suggests that OCT mitigates LPS-induced endothelial cell and lung injury, suggesting that it may represent an exciting therapeutic possibility in diseases related to barrier dysfunction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560538PMC
http://dx.doi.org/10.1016/j.cellsig.2024.111455DOI Listing

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