Ischemia postconditioning preventing lung ischemia-reperfusion injury
| Autor: | Wei-Qin Yang, Song-Bo Di, Qifeng Cao, Dan-Ping Wang, Ming-Hui Zhang, Mei-Jun Qu |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Fas Ligand Protein Interleukin-1beta Ischemia Apoptosis Pharmacology Lung injury Biology Antioxidants Dexamethasone Proinflammatory cytokine Rats Sprague-Dawley Malondialdehyde Genetics medicine Animals fas Receptor Rats Wistar Ischemic Postconditioning Lung Peroxidase bcl-2-Associated X Protein Inflammation Caspase 3 Interleukin-6 Tumor Necrosis Factor-alpha General Medicine Free Radical Scavengers medicine.disease Rats medicine.anatomical_structure Reperfusion Injury Perfusion Reperfusion injury medicine.drug |
| Zdroj: | Gene. 554(1) |
| ISSN: | 1879-0038 |
| Popis: | 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 p0.05 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 p0.05 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. |
| Databáze: | OpenAIRE |
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