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

Figure 2.

Figure 2

Upregulation of NOX1, NOX2, and NOX4 in ACS exposed mouse lungs; and reduced expression of NOXs in mice genetically silenced for each isoform. Mice were subjected to CS or filtered air for 1 h and then harvested at 6 h. The protein expression of NOX isoforms NOX1, NOX2, and NOX4 was determined in the lungs of mice exposed to ACS, mice knocked down of NOX1 or NOX4, and NOX2 knockout mice using Western blotting analyses. (A–C) Representative Western blots and grouped data of NOX1, NOX2, or NOX4 protein expression in ACS exposed mouse lungs. The data indicate that protein expression of NOX1, NOX2, and NOX4 was significantly upregulated in ACS exposed mouse lungs. (D–F) Representative Western blots and grouped data of NOX1, NOX2, or NOX4 expression in mice silenced for each isoform. The data indicate that RNAi-mediated NOX1 or NOX4 knockdown significantly attenuated NOX1 or NOX4 protein abundance respectively, while NOX2 was not detected in the lungs of NOX2−/y mice. All data are presented as Mean ± SEM, n = 3–4. * p < 0.05, ** p < 0.01 vs. air exposed control group.