Abstract
Morphological and functional abnormalities of vascular endothelial cells (VECs) are risk factors of ischemia-reperfusion in skin flaps. Signaling pathway mediated by interleukin-1 receptor (IL-1R) is essential to hypoxia/reoxygenation (H/R) injury of VECs. While the TIR/BB-loop mimetic (AS-1) disrupts the interaction between IL-1R and myeloid differentiation primary-response protein 88 (MyD88), its role in the VECs dysfunction under H/R is unclear. In this study, we first showed that there was an infiltration of inflammatory cells and the apoptosis of VECs by using a skin flap section from patients who received flap transplantation. We then showed that the H/R treatment induced apoptosis and loss of cell migration of endothelial cell line H926 were attenuated by AS-1. Furthermore, our data suggested that AS-1 inhibits the interaction between IL-1R and MyD88, and subsequent phosphorylation of IκB and p38 pathway, as well as the nuclear localization of NF-KB subunit p65/p50. Thus, this study indicated that the protective role of AS-1 in H/R induced cellular injury may be due to the AS-1 mediated down-regulation of IL-1R signaling pathway.
Highlights
Flap transplantation is commonly used to repair tissue defect and reconstruct organs
AS-1 ameliorated the viability of vascular endothelial cell injured by H/R
The vascular endothelial cells were stimulated by AS-1 at different concentrations for 72 hours
Summary
Flap transplantation is commonly used to repair tissue defect and reconstruct organs. The transplanted flaps (random, axial, or free) may undergo ischemia and reperfusion, a complex pathophysiological process of injury. Experimental studies have shown that oxygen free radical damage and calcium overload can cause vascular endothelial apoptosis, inflammatory response and other lesions, all contribute to ischemia-reperfusion injury[1,2,3]. Vascular endothelial cells participate in various physiological activities, such as synthesizing biological substances, contracting blood vessels, maneuvering blood flow, activating blood coagulation and regulating platelet aggregation[4,5,6,7]. Ischemia-reperfusion (I/R) can inflict endothelial cells with morphological and functional abnormalities, such as apoptosis, inflammatory substance synthesis[8,9]. As a key mediator in immune and inflammatory responses, IL-1 undergoes its signaling pathway through the activation of interleukin-1 receptor
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