Treatment with hydrogen molecule attenuates cardiac dysfunction in streptozotocin-induced diabetic mice.

Abstract

Adult male mice received streptozotocin (50 mg/kg/day intraperitoneally for 5 days) to establish a diabetic model, followed by 8 weeks of hydrogen-rich water (1.3±0.2 mg/L) administration. Despite no significant change in blood glucose, cardiac hypertrophy markers (atrial natriuretic factor, β-myosin heavy chain) and fibrosis markers (collagen I/III, TGF-β, α-smooth muscle actin, osteopontin) were markedly reduced. Apoptotic indicators including caspase-3 activity and Bax/Bcl-2 ratio also declined. Cardiac function improved alongside reductions in oxidative stress, inflammatory signaling, and endoplasmic reticulum stress. Suppression of JNK, p38 MAPK, and NF-κB pathways was observed in cardiac tissue, suggesting these mechanisms underlie the cardioprotective effects of molecular hydrogen independent of glycemic control.

Mechanism

Hydrogen-rich water suppresses JNK, p38 MAPK, and NF-κB signaling pathways, thereby reducing oxidative stress, inflammation, and endoplasmic reticulum stress, which collectively attenuate cardiac hypertrophy, fibrosis, and apoptosis in diabetic hearts.