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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. 4. — Effects of NOX4 on PICs and effects of blocking PIC on TRPA1 expression. (a) LIRI amplified the levels of PICs (IL-1β, IL-6, and TNF-α) in the cNTS as compared with sham controls. *P < 0.05, LIRI rats (n = 12) versus sham control rats (n = 12). However, inhibition of NOX4 by ICV administration of GKT137831 (GKT) did not alter significantly the amplified levels of IL-1β, IL-6, and TNF-α in the cNTS of LIRI rats (n = 8). P > 0.05 between LIRI rats and LIRI rats with inhibitor. (b) Inhibition of PIC signals by respective ICV infusion of IL-1Ra (IL-1R inhibitor), TCZB (IL-6R inhibitor), and ETAN (TNFR inhibitor) attenuated upregulation of TRPA1 in the cNTS induced by LIRI. *P < 0.05, LIRI rats (n = 10) versus sham control rats (n = 6) and LIRI rats with each inhibitor (n = 8 in each group). ETAN: etanercept; GKT: GKT137831; IL-1Ra: IL-1R receptor inhibitor; LIRI: lung ischemia–reperfusion injury; TCZB: tocilizumab; TRPA1: transient receptor potential ankyrin 1.