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. 2021 Nov 12;11(4):20458940211059712. doi: 10.1177/20458940211059712

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© The Author(s) 2021

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://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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Figure 2. — Boxplot depiction of right ventricular systolic pressure (RVP, Panel a) and right ventricular/left ventricle + septum ratio- (RV/LV+S, Panel b) in adult Sprague Dawley rats exposed to room air (control rats), to hypoxia/Sugen (three weeks hypoxia exposure, three weeks Sugen), and to hypoxia/Sugen while receiving IP delivery of eNAMPT mAb (1 mg/kg). Both hemodynamic parameters at six weeks were significantly elevated in hypoxia/Sugen-exposed rat group whereas rats treated with the eNAMPT-neutralizing mAb showed a significant reduction in both RVP and RV/LV+S in comparison to non-treated group. (c–e) Plasma levels of eNAMPT (c) Interleukin-6 or IL-6 (d), and TNF-α (e) were assessed in the three studied rat groups and revealed significant increases in each inflammatory mediator in hypoxia/Sugen-exposed rats compared with room air controls. Hypoxia/Sugen-exposed rats receiving the eNAMPT mAb exhibited marked reductions in each cytokine at six weeks. N= 5/groups. Bars represents mean ± SE. *p<0.05 vs. RA controls; ** p<0.05 vs. hypoxia/Sugen-exposed untreated rats.