Background: Lung ischemia-reperfusion injury (LIRI) is a major complication after lung transplantation. Annexin A1 (AnxA1) ameliorates inflammation in various injured organs. This study aimed to determine the effects and mechanism of AnxA1 on LIRI after lung transplantation.
Methods: Thirty-two rats were randomized into sham, saline, Ac2-26 and Ac2-26/L groups. Rats in the saline, Ac2-26 and Ac2-26/L groups underwent left lung transplantation and received saline, Ac2-26, and Ac2-26/L-NIO, respectively. After 24 h of reperfusion, serum and transplanted lung tissues were examined.
Results: The partial pressure of oxygen (PaO) was increased in the Ac2-26 group compared to that in the saline group but was decreased by L-NIO treatment. In the Ac2-26 group, the wet-to-dry (W/D) weight ratios, total protein concentrations, proinflammatory factors and inducible nitric oxide synthase levels were notably decreased, but the concentrations of anti-inflammatory factors and endothelial nitric oxide synthase levels were significantly increased. Ac2-26 attenuated histological injury and cell apoptosis, and this improvement was reversed by L-NIO.
Conclusions: Ac2-26 reduced LIRI and improved alveoli-capillary permeability by inhibiting oxygen stress, inflammation and apoptosis. The protective effect of Ac2-26 on LIRI largely depended on the endothelial nitric oxide synthase pathway.
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[Annexin A1 activates the G protein-coupled formyl peptide receptor type 2-dependent endothelial nitric oxide synthase pathway to alleviate sepsis associated acute lung injury].
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
September 2024
Department of Critical Care Medicine, the Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou, China. Corresponding author: Qin Song, Email:
Article Synopsis
- The study aimed to determine if annexin A1 (ANXA1) helps improve lung injury caused by sepsis through the activation of the FPR2-dependent eNOS pathway.
- A total of 24 male SD rats were divided into four groups for experimentation, including a control group, a lipopolysaccharide (LPS) induced lung injury group, and two groups treated with ANXA1 mimetics with and without a FPR2 inhibitor.
- Results indicated that rats treated with the ANXA1 mimetic showed less inflammation and improved lung tissue, while the FPR2 inhibitor group exhibited more severe inflammation, highlighting ANXA1's protective role against sepsis-induced lung injury.
Ac2-26 Reduced Lung Injury After Cardiopulmonary Bypass via the AKT1/GSK3β/eNOS Pathway.
J Surg Res
September 2024
Department of Intensive Care Unit, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. Electronic address:
Introduction: Cardiopulmonary bypass (CPB) leads to severe inflammation and lung injury. Our previous study showed that Ac2-26 (an active n-terminal peptide of Annexin A1) can reduce acute lung injury. The aim of this study was to evaluate the effect of Ac2-26 on lung injury in CPB rats.
View Article and Find Full Text PDFAc2-26 reduced the liver injury after cardiopulmonary bypass in rats via AKT1/GSK3β/eNOS pathway.
J Cardiothorac Surg
June 2024
Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, 246Xuefu Road, Harbin, 150081, Heilongjiang, China.
Objective: About 10% of patients after cardiopulmonary bypass (CPB) would undergo acute liver injury, which aggravated the mortality of patients. Ac2-26 has been demonstrated to ameliorate organic injury by inhibiting inflammation. The present study aims to evaluate the effect and mechanism of Ac2-26 on acute liver injury after CPB.
View Article and Find Full Text PDFAc2-26 activated the AKT1/GSK3β pathway to reduce cerebral neurons pyroptosis and improve cerebral function in rats after cardiopulmonary bypass.
BMC Cardiovasc Disord
May 2024
Department of Anesthesiology, Hainan General Hospital (Hainan Affiliated Hosptial of Hainan Medical University), Clinical College, Hainan Medical University, Haikou, 570311, China.
Background: Cardiopulmonary bypass (CPB) results in brain injury, which is primarily caused by inflammation. Ac2-26 protects against ischemic or hemorrhage brain injury. The present study was to explore the effect and mechanism of Ac2-26 on brain injury in CPB rats.
View Article and Find Full Text PDFPurpose: Although mechanical ventilation is an essential support for acute respiratory distress syndrome (ARDS), ventilation also leads to ventilator-induced lung injury (VILI). This study aimed to estimate the effect and mechanism of Annexin A1 peptide (Ac2-26) on VILI in ARDS rats.
Methods: Thirty-two rats were randomized into the sham (S), mechanical ventilation (V), mechanical ventilation/Ac2-26 (VA), and mechanical ventilation/Ac2-26/L-NIO (VAL) groups.
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