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. 2014 Nov 14;5:440. doi: 10.3389/fphys.2014.00440

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Copyright © 2014 Liu, Lin, Lu, Peng, Lee and Kou.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Eicosapentaenoic acid (EPA) attenuates cigarette smoke (CS)-induced increases in pro-inflammatory chemokines and malondialdehyde in lung tissues sampled from mice. Levels of macrophage inflammatory protein 2 (MIP-2) (A), monocyte chemoattractant protein-1 (MCP-1) (B) and keratinocyte chemoattractant (KC) (C) in lung tissues were analyzed by ELISA. Levels of malondialdehyde (MDA) (D) were measured by an assay kit and served as an indication of oxidative stress. Data in each group are mean ± s.e.m. from 6 mice. ^*p < 0.05 vs. the air-exposure group; ^#p < 0.05 vs. the CS-exposure group with vehicle treatment. See the legend of Figure 1 for detailed information on each study group.