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. 2020 Feb 6;10:1962. doi: 10.1038/s41598-020-58999-0

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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H₂ relieves OVA sensitization and challenge-induced suppression of NAD production. Mice in Con, HRS, OVA or OVA + HRS group were sensitized and challenged, or/and treated with HRS as described above. Lung mitochondrial levels of nicotinamide adenine dinucleotide (NAD), NAD/NADH ratio and nicotinamide phosphoribosyltransferase (NAMPT) content were measured. Means ± SEM of 5 mice per group. *p < 0.05, compared to control group. ^#p < 0.05, compared to OVA group (one-way ANOVA). (A) Lung mitochondrial NAD production. (B) Lung mitochondrial NAD/NADH ratio. (C) Lung mitochondrial NAMPT expression.