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Published on: May 28, 2019
Ischemia postconditioning preventing lung ischemia-reperfusion injury
Qi-Feng Cao1, Mei-Jun Qu1, Wei-Qin Yang1
13rd Department of Internal Medicine, Integrated Chinese and Western Medicine Hospital of Taizhou, Zhejiang Province 317523, China.
Objective:
This study evaluates the inhibitory effect of IPO against ischemia reperfusion (I/R) induced lung injury in rats.
Methods:
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.
Results:
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.
Conclusion:
Postconditioning obviously inhibits I/R induced lung injury by its antioxidant, anti-inflammatory and anti-apoptosis activities.
