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. 2013 Sep 10;8(9):e74742. doi: 10.1371/journal.pone.0074742

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© 2013 Wu et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Hypercapnic acidosis (HCA) increased the IκB-α level and reduced cytoplasmic phosphorylated IKK and nuclear NF-κB p65 levels in ischemia-reperfusion (IR)-induced lung injury. Zinc protoporphyrin IX (ZnPP) treatment partially attenuated the protective effect of HCA. TATA and β-actin served as loading controls for nuclear and cytoplasmic proteins, respectively. A representative blot is shown. Data are expressed as mean ± SD. *significantly different from control (P < 0.05); +significantly different from IR-vehicle (P < 0.05); ^# significantly different from IR+HCA (P < 0.05), using one-way ANOVA with Bonferroni post-test.