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. 2019 Aug 2;9(3):2045894019865169. doi: 10.1177/2045894019865169

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© The Author(s) 2019

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Fig. 3. — Effects of NOX4 on products of oxidative stress and expression of TRPA1. (a) LIRI amplified the levels of oxidative products 8-iso PGF2α and 8-OHdG in the cNTS. As NOX-4 inhibitor GKT137831 (GKT) was infused via ICV, increases of 8-iso PGF2α and 8-OHdG were attenuated. *P < 0.05, LIRI rats (n = 16) versus sham control rats (n = 15) and LIRI rats with inhibitor (n = 12). (b) The protein levels of TRPA1 were amplified in the cNTS tissues of LIRI rats and inhibition of NOX4 by ICV administration of GKT137831 decreased expression of TRPA1 in the cNTS of LIRI rats. *P < 0.05, LIRI rats (n = 12) versus sham control rats (n = 8) and LIRI rats with inhibitor (n = 10). GKT: GKT137831; LIRI: lung ischemia–reperfusion injury; TRPA1: transient receptor potential ankyrin 1.