Hydrogen ameliorates pulmonary hypertension in rats by anti-inflammatory and antioxidant effects.

Abstract

Pulmonary arterial hypertension (PAH) involves reactive oxygen species and inflammatory processes in its pathogenesis. This study examined the effects of hydrogen-saturated water in a monocrotaline (MCT)-induced PAH rat model. Male Sprague-Dawley rats were divided into three groups: MCT plus hydrogen-saturated water, MCT plus dehydrogenized water, and saline plus dehydrogenized water. Hemodynamic assessment and morphometric pulmonary vascular analysis were performed 16 days after substance administration. Compared with the MCT-only group, hydrogen-treated animals showed significantly reduced pulmonary arterial pressure, preserved vascular density, decreased adventitial macrophage accumulation, lower 8-hydroxy-deoxyguanosine-positive cell counts, and reduced expression of stromal cell-derived factor-1 and monocyte chemoattractant protein-1. Phosphorylated STAT3 and NFAT expression levels were also markedly lower in the hydrogen group. These findings indicate that hydrogen-rich water intake attenuates MCT-induced PAH through suppression of oxidative stress, macrophage infiltration, and modulation of the STAT3/NFAT signaling axis.

Mechanism

Hydrogen-rich water intake suppressed macrophage accumulation in the pulmonary adventitia, reduced oxidative DNA damage (8-OHdG), and downregulated phosphorylated STAT3 and NFAT expression, collectively attenuating MCT-induced pulmonary arterial hypertension.