Ischemia postconditioning preventing lung ischemia–reperfusion injury

• Published in: Gene Vol. 554; no. 1; pp. 120 - 124
• Main Authors: Cao, Qi-Feng, Qu, Mei-Jun, Yang, Wei-Qin, Wang, Dan-Ping, Zhang, Ming-Hui, Di, Song-Bo
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.01.2015
• Subjects: Animals; Antioxidant; Antioxidants - metabolism; Apoptosis; bcl-2-Associated X Protein - metabolism; Caspase 3 - metabolism; Dexamethasone - chemistry; Fas Ligand Protein - metabolism; fas Receptor - metabolism; Free Radical Scavengers; Inflammation; Interleukin-1beta - metabolism; Interleukin-6 - metabolism; Ischemic Postconditioning; Lung - metabolism; Lung ischemia reperfusion; Male; Malondialdehyde - metabolism; Peroxidase - metabolism; Rats; Rats, Sprague-Dawley; Rats, Wistar; Reperfusion Injury - prevention & control; Tumor Necrosis Factor-alpha - metabolism; IPO; Lung ischemia reperfusion; Ischemic postconditioning; Antioxidant; I/R; IPC
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2014.10.009

This study evaluates the inhibitory effect of IPO against ischemia reperfusion (I/R) induced lung injury in rats. Anesthetized and mechanically ventilated adult Sprague–Dawley rats were randomly assigned to one of the following groups (n=12 each): the sham operated control group, the ischemia–reperfusion (IR) group (30min of left-lung ischemia and 24h of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion), and the dexamethasone plus IPO group (rats were injected with dexamethasone (3mg/kg·day−1) 10min prior to the experiment and the rest of the procedures were the same as the IPO group). Lung injury was assessed by wet-to-dry lung weight ratio and tissue apoptosis and biochemical changes. Lung ischemia–reperfusion increased lung MDA production, serum proinflammatory cytokine count, and MPO activity and reduced antioxidant enzyme activities (all p<0.05 I/R versus sham), accompanied with a compensatory increase in caspase-3, bax, Fas, FasL proteins and a decrease in Bcl-2 protein. Plasma levels of TNF-α, IL-6, and IL-1β were increased in the I/R group (all p<0.05 versus sham). IPO attenuated or prevented all the above changes. Treatment with dexamethasone enhanced all the protective effects of postconditioning. Postconditioning obviously inhibits I/R induced lung injury by its antioxidant, anti-inflammatory and anti-apoptosis activities.