Ischemia postconditioning preventing lung ischemia–reperfusion injury

ObjectiveThis study evaluates the inhibitory effect of IPO against ischemia reperfusion (I/R) induced lung injury in rats.MethodsAnesthetized 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 (30 min of left-lung ischemia and 24 h 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 (3 mg/kg·day− 1) 10 min 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.ResultsLung 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.ConclusionPostconditioning obviously inhibits I/R induced lung injury by its antioxidant, anti-inflammatory and anti-apoptosis activities.