Consumption of hydrogen-rich water ameliorates atherosclerosis by modulating gut microbiota and enhancing short-chain fatty acid levels.

Abstract

Using ApoE-knockout mice as an atherosclerosis model, this study examined how hydrogen-rich water (HW) consumption affects plaque development and vascular stability. HW-fed animals showed marked reductions in plaque burden alongside altered gut microbial community structure and modified short-chain fatty acid (SCFA) profiles. Antibiotic-mediated microbiota depletion eliminated the protective phenotype, whereas fecal microbiota transplantation from HW-treated donors reproduced anti-atherosclerotic effects in recipient mice, confirming a gut microbiota-dependent mechanism. Propionate concentrations rose significantly in both cecal contents and serum of HW-treated animals. In vitro experiments demonstrated that propionate directly inhibited M1 macrophage polarization and attenuated inflammatory signaling. Collectively, the findings identify a gut microbiota–propionate–macrophage axis as a central pathway through which HW reduces vascular inflammation and plaque progression.

Mechanism

HW reshapes gut microbial composition, elevating propionate levels in cecal contents and serum; propionate in turn suppresses M1 macrophage polarization and inflammatory signaling, thereby reducing atherosclerotic plaque formation and improving plaque stability.