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Published on: May 21, 2018
Lanreotide protects against LPS-induced inflammation in endothelial cells and mouse lungs
Md Matiur Rahman Sarker1, Saikat Fakir1, Khadeja-Tul Kubra1
1School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA, USA.
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.
Insights
Lanreotide (LAN) effectively reduces inflammation and injury in endothelial cells and mice caused by bacterial endotoxins (LPS). This synthetic somatostatin analog shows promise in mitigating acute lung injury and related cellular damage.
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- Somatostatin regulates Growth Hormone and is used clinically for neuroendocrine tumors and acromegaly.
- Synthetic somatostatin analogs are increasingly recognized for their anti-inflammatory properties.
- Lipopolysaccharide (LPS) triggers significant inflammatory responses and injury in endothelial cells and tissues.
Purpose of the Study:
- To investigate the protective effects of Lanreotide (LAN) against LPS-induced injury in endothelial cells and a mouse model.
- To determine LAN's impact on endothelial hyperpermeability, inflammation, and reactive oxygen species (ROS) generation.
- To evaluate LAN's efficacy in mitigating LPS-induced acute lung injury, including edema and inflammatory signaling pathways.
Main Methods:
- In vitro studies using bovine pulmonary artery endothelial cells (BPAEC) and human lung microvascular endothelial cells (HULEC-5a) exposed to LPS.
- In vivo studies using a murine model of LPS-induced acute lung injury.
- Assessment of endothelial barrier function, ROS production, inflammatory markers, and specific signaling pathway activation (MLC2, Cofilin, ERK1/2, STAT1, STAT3, P38).
Main Results:
- Lanreotide (LAN) significantly reduced LPS-induced hyperpermeability, inflammation, and ROS generation in endothelial cells.
- LAN treatment mitigated lung edema and suppressed key inflammatory signaling pathways (MLC2, Cofilin, ERK1/2, STAT1, STAT3, P38) in the LPS-induced acute lung injury mouse model.
- These findings demonstrate LAN's potent anti-inflammatory and protective effects against endotoxin-induced cellular and tissue damage.
Conclusions:
- Lanreotide (LAN) effectively counteracts experimental LPS-induced injury in endothelial cells and mice.
- LAN exhibits significant anti-inflammatory and protective properties against acute lung injury.
- The study supports the therapeutic potential of Lanreotide in conditions involving endotoxin-mediated inflammation and endothelial dysfunction.
