Abstract
Lung ischemia-reperfusion injury (LIRI) is still an unsolved medical issue, which negatively affects the prognosis of many lung diseases. The aim of this study is to determine the effects of RvD1 on LIRI and the potential mechanisms involved. The results revealed that the levels of complement, immunoglobulin, cytokines, sICAM-1, MPO, MDA, CINC-1, MCP-1, ANXA-1, TLR4, NF-κBp65, apoptosis index, and pulmonary permeability index were increased, whereas the levels of SOD, GSH-PX activity, and oxygenation index were decreased in rats with LIRI. Except for ANXA-1, these responses induced by LIRI were significantly inhibited by RvD1 treatment. In addition, LIRI-induced structure damages of lung tissues were also alleviated by RvD1 as shown by H&E staining and transmission electron microscopy. The results suggest that RvD1 may play an important role in protection of LIRI via inhibition of complement, immunoglobulin, and neutrophil activation; down-regulation of TLR4/NF-κB; and the expression of a variety of inflammatory factors.Electronic supplementary materialThe online version of this article (doi:10.1007/s10753-016-0364-9) contains supplementary material, which is available to authorized users.
Highlights
Lung ischemia–reperfusion injury (LIRI) is still an unsolved medical issue both in research and clinic [1, 2]
We found that the levels of IgM and IgG and the complements C1q, C2, C3a, C4, and C5a were increased by LIRI
Our results showed that the cytokines levels of IL1β, IL-6, Tumor necrosis factor (TNF)-α, and Soluble intercellular adhesion molecule (sICAM)-1; inflammatory factors levels of cytokine-induced neutrophil chemoattractant (CINC)-1, monocyte chemoattractant protein (MCP)-1, and ANXA-1; and the messenger RNA (mRNA) level and protein expression of toll-like receptor 4 (TLR4) and NFκBp65 were up-regulated under LIRI
Summary
Lung ischemia–reperfusion injury (LIRI) is still an unsolved medical issue both in research and clinic [1, 2]. The pathogenesis of LIRI has been studied for many years. In this respect, oxygen radicals, inflammatory mediators, and neutrophils have been identified to play important roles in ischemia–reperfusion injury (IRI) [5]. LIRI has been considered as a congenital autoimmune reaction [6]. Ischemia-exposed antigens on the membrane could bind with the toll-like receptor 4 (TLR4) during reperfusion and activate the related immune response [7]. The ischemic antigen could bind with the plasma-specific immunoglobulin and form immune complexes to promote the inflammatory reaction and aggravate the lung injury [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
