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. 2022 Aug 8;11(8):1539. doi: 10.3390/antiox11081539

Figure 3.

Figure 3

Knockdown of NOX1, NOX2, or NOX4 significantly attenuated ACS induced ROS production in the mouse lung. Mice were exposed to CS or filtered air for 1 h and harvested at 6 h. Frozen lung OCT sections from the superior lobe of the right lung were stained with dihydroethidium (DHE) for detection of ROS production. (A,B) Representative images and quantitative data of DHE fluorescent imaging of lung tissue sections from ACS exposed mice with or without RNAi-mediated knockdown of NOX1 or NOX4. The data indicate significantly increased ROS production in ACS exposed mice, which was markedly attenuated by RNAi-mediated in vivo silencing of NOX1 or NOX4. (C,D) Representative images and grouped data of DHE fluorescent imaging of lung tissue sections from ACS exposed wildtype (WT) mice and NOX2−/y mice. The data indicate significantly increased ROS production in ACS exposed WT mice, which was markedly attenuated in NOX2−/y mice. All data are presented as Mean ± SEM, n = 6. Scale bar, 100 µm. ** p < 0.01, *** p < 0.001 vs. air exposed control group. ### p < 0.001 vs. ACS exposed group.