Ss of ischemia eperfusion injury (IRI) [7]. Studies have demonstrated that the protection of the energy status and the amelioration?2016 Zhao et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if order LDN193189 changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/ publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Zhao et al. J Transl Med (2016) 14:Page 2 ofof metabolic disorders could remarkably reduce the organ IRI [8, 9]. Nevertheless, the energy metabolism of LIRI has its own characteristics, and there has been little research in this new area. The endogenous lipid mediators, such as resolvin (Rv) and lipoxin, have been confirmed to have the anti-inflammatory effect in many studies [10, 11]. These specialized pro-resolving mediators have conserved structures with many functions in host defense, pain, organ protection and tissue remodeling [12]. In addition, these bioactive substances have been found to have a protective effect on organ ischemia reperfusion injury [13?9]. Recently, it has been reported that RvD1 could preserve the activity of Na+ +-buy CEP-37440 ATPase and relieve the lung injury induced by oxidative stress and inflammatory PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28854080 response [20, 21]; however, little research has been reported about the effect of RvD1 on the energy metabolism of LIRI. In this study, we aim to investigate the protective effect and the related mechanisms of RvD1 on the lung energy metabolism caused by LIRI in rats, and hope to provide a new idea and its experimental evidence for the treatment of LIRI. In particularly, through the intravenous injection of RvD1, we studied the effects of RvD1 on the ATP, ADP, glycogen, lactic acid content, the activity of Na+?K+-ATPase, the inflammatory response and the oxidative stress in lung tissue. Meanwhile, the pathological changes, apoptosis rate and pulmonary function in the lung tissue were also evaluated.clamped left hilum was clearly exposed by slightly stirring up the clamp. Before blocking, heparin was injected by i.v. (1 mg/kg body weight). After ischemia for 45 min, the artery clamp was removed (no blocking in sham group) and then reperfusion was started and lasted for 150 min. During the reperfusion time, 0.5 ml normal saline (NS) was injected by i.v. every hour to maintain the body fluid. Finally, after the chest wall was closed and the body temperature was maintained using a 37 warming plate.Animal grouping and treatmentsMethodsRat model of LIRIResolvin D1 (RvD1, C22H32O5, 7S,8R,17S-trihydroxy4Z,9E,11E,13Z,15E,19Z-docosahexaenoic acid, please see Additional file 1: Figure S1 in the Supplementary Material) was purchased from Cayman Chemical Company (Ann Arbor, USA). Forty SD rats were randomly divided into four groups (10 rats/group) as follows: (1) Sham group: no blocking of hilum of left lung after thoracotomy; (2) untreated IR control (IR-C) group: blocking of hilum of left lung after thoracotomy for 45 min, followed by reperfusion for 150 min; (3) IR treated with normal saline (IR-NS) group: after blocking the hilum of left lung for 45 min, reperfusion for 10 min then injection 2 ml/kg NS by formal v.Ss of ischemia eperfusion injury (IRI) [7]. Studies have demonstrated that the protection of the energy status and the amelioration?2016 Zhao et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/ publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Zhao et al. J Transl Med (2016) 14:Page 2 ofof metabolic disorders could remarkably reduce the organ IRI [8, 9]. Nevertheless, the energy metabolism of LIRI has its own characteristics, and there has been little research in this new area. The endogenous lipid mediators, such as resolvin (Rv) and lipoxin, have been confirmed to have the anti-inflammatory effect in many studies [10, 11]. These specialized pro-resolving mediators have conserved structures with many functions in host defense, pain, organ protection and tissue remodeling [12]. In addition, these bioactive substances have been found to have a protective effect on organ ischemia reperfusion injury [13?9]. Recently, it has been reported that RvD1 could preserve the activity of Na+ +-ATPase and relieve the lung injury induced by oxidative stress and inflammatory PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28854080 response [20, 21]; however, little research has been reported about the effect of RvD1 on the energy metabolism of LIRI. In this study, we aim to investigate the protective effect and the related mechanisms of RvD1 on the lung energy metabolism caused by LIRI in rats, and hope to provide a new idea and its experimental evidence for the treatment of LIRI. In particularly, through the intravenous injection of RvD1, we studied the effects of RvD1 on the ATP, ADP, glycogen, lactic acid content, the activity of Na+?K+-ATPase, the inflammatory response and the oxidative stress in lung tissue. Meanwhile, the pathological changes, apoptosis rate and pulmonary function in the lung tissue were also evaluated.clamped left hilum was clearly exposed by slightly stirring up the clamp. Before blocking, heparin was injected by i.v. (1 mg/kg body weight). After ischemia for 45 min, the artery clamp was removed (no blocking in sham group) and then reperfusion was started and lasted for 150 min. During the reperfusion time, 0.5 ml normal saline (NS) was injected by i.v. every hour to maintain the body fluid. Finally, after the chest wall was closed and the body temperature was maintained using a 37 warming plate.Animal grouping and treatmentsMethodsRat model of LIRIResolvin D1 (RvD1, C22H32O5, 7S,8R,17S-trihydroxy4Z,9E,11E,13Z,15E,19Z-docosahexaenoic acid, please see Additional file 1: Figure S1 in the Supplementary Material) was purchased from Cayman Chemical Company (Ann Arbor, USA). Forty SD rats were randomly divided into four groups (10 rats/group) as follows: (1) Sham group: no blocking of hilum of left lung after thoracotomy; (2) untreated IR control (IR-C) group: blocking of hilum of left lung after thoracotomy for 45 min, followed by reperfusion for 150 min; (3) IR treated with normal saline (IR-NS) group: after blocking the hilum of left lung for 45 min, reperfusion for 10 min then injection 2 ml/kg NS by formal v.
