Life sciences · 2026
Inhalation of hydrogen gas reduces exacerbations of acute aortic dissection in mice.
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Iketani Masumi, Kawata Mitsuhiro, Ito Masafumi, Ohsawa Ikuroh, Takayama Kenichi, Aokage Toshiyuki
Аннотация
AIMS: Acute aortic dissection (AAD) is a life-threatening condition in which vascular inflammation contributes to disease progression and complications such as aortic rupture. Current treatment is centered on hemodynamic control, and anti-inflammatory options remain limited. We investigated whether inhaled molecular hydrogen (H2) gas attenuates AAD severity in a murine model.
MATERIALS AND METHODS: AAD was induced in male C57BL/6J mice by β-aminopropionitrile pretreatment followed by continuous angiotensin II infusion. Mice were exposed to 2% H2 gas or control gas for 24 h, and effects on AAD severity and inflammation were examined.
KEY FINDINGS: H2 inhalation improved 24-h survival and spontaneous locomotor activity, while systolic blood pressure was not altered. H2 also reduced aortic rupture frequency and suppressed false lumen enlargement. In plasma, H2 inhalation significantly reduced IL-6 and G-CSF levels, while MMP-9 and CXCL1 showed downward trends. In the aortic wall, H2 reduced MMP-9 and CXCL1 expression, including within Ly-6B.2-positive regions, whereas CXCL1 expression within SMA-positive regions was unchanged. In addition, the number of Ly-6B.2-positive cells in the aortic wall was decreased and positively correlated with false lumen area. In bone marrow, the reduction in CD11b+Ly-6G+ neutrophils observed in AAD mice was significantly attenuated by H2 inhalation. H2 also attenuated oxidative stress-related changes in the aortic wall.
SIGNIFICANCE: These findings indicate that 2% H2 gas inhalation reduces acute AAD exacerbation without affecting blood pressure, likely through modulation of inflammatory mediators and neutrophil-associated acute inflammation. H2 inhalation may represent a safe adjunctive strategy to limit AAD progression and rupture.
MATERIALS AND METHODS: AAD was induced in male C57BL/6J mice by β-aminopropionitrile pretreatment followed by continuous angiotensin II infusion. Mice were exposed to 2% H2 gas or control gas for 24 h, and effects on AAD severity and inflammation were examined.
KEY FINDINGS: H2 inhalation improved 24-h survival and spontaneous locomotor activity, while systolic blood pressure was not altered. H2 also reduced aortic rupture frequency and suppressed false lumen enlargement. In plasma, H2 inhalation significantly reduced IL-6 and G-CSF levels, while MMP-9 and CXCL1 showed downward trends. In the aortic wall, H2 reduced MMP-9 and CXCL1 expression, including within Ly-6B.2-positive regions, whereas CXCL1 expression within SMA-positive regions was unchanged. In addition, the number of Ly-6B.2-positive cells in the aortic wall was decreased and positively correlated with false lumen area. In bone marrow, the reduction in CD11b+Ly-6G+ neutrophils observed in AAD mice was significantly attenuated by H2 inhalation. H2 also attenuated oxidative stress-related changes in the aortic wall.
SIGNIFICANCE: These findings indicate that 2% H2 gas inhalation reduces acute AAD exacerbation without affecting blood pressure, likely through modulation of inflammatory mediators and neutrophil-associated acute inflammation. H2 inhalation may represent a safe adjunctive strategy to limit AAD progression and rupture.