Abstract
IRW (Ile-Arg-Trp), a bioactive peptide isolated from egg ovotransferrin, has been shown to exert anti-inflammatory effects. In this study, the effects of IRW on inflammatory cytokines and microbiota were explored in human umbilical vein endothelial cells (HUVECs) and a lipopolysaccharide (LPS)-induced rat model of inflammatory peritonitis. Rats were injected intraperitoneally with LPS to establish peritonitis. HUVECs were exposed to IRW for 12 h before introducing LPS. Notably, IRW exerted beneficial effects against LPS-induced peritonitis, specifically, by reducing the serum levels of tumour necrosis factor (TNF)-α and interleukin (IL)-6 and myeloperoxidase (MPO) activity (P<0.05). A faecal microbiota analysis revealed that IRW significantly increased the Shannon and decreased the Simpson indices (P<0.05). Furthermore, IRW treatment significantly inhibited the LPS-induced enhancement of TNF-α, IL-8, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression in HUVECs (P<0.05). In conclusion, IRW supplementation inhibited the inflammatory mediator synthesis and LPS-induced inflammatory responses and influenced the gut microbiota.
Highlights
In several diseases, including atherosclerosis, cancer, diabetes mellitus, endotoxic shock, and thrombosis, the pathogenesis is modulated by endothelial cell inflammatory responses [1, 2]
This study explored the anti-inflammatory effects of IRW in an LPS-induced rat model of peritonitis and human umbilical vein endothelial cells (HUVECs)
This study explored the anti-inflammatory effects of IRW, a tripeptide derived from ovotransferrin, on HUVEC cells and endothelial cells from rats with LPS-induced peritonitis
Summary
In several diseases, including atherosclerosis, cancer, diabetes mellitus, endotoxic shock, and thrombosis, the pathogenesis is modulated by endothelial cell inflammatory responses [1, 2]. LPS stimulates Toll-like receptor 4 (TLR4) on the surfaces of immune cells to initiate a cascade of downstream signals in human vascular endothelial cells. This cascade leads to the uncontrolled production of cytokines, including tumour necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8, as well as adhesion molecules such as intercellular cell adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) [6, 7]. The overproduction of these cytokines induces vascular inflammation [8]. Inhibiting either the synthesis or release of these inflammatory mediators may limit inflammatory disease
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