Abstract
Aims. The study was designed to explore whether hydrogen sulphide (H(2)S) and nitric oxide (NO) generation changed in D-galactose- (D-gal-) induced ageing, the possible effects of exogenous H(2)S supplementation, and related mechanisms. Results. In D-gal-induced senescent mice, both H(2)S and NO levels in the heart, liver, and kidney tissues were decreased significantly. A similar trend was observed in D-gal-challenged human umbilical vein endothelial cells (HUVECs). Sustained H(2)S donor (NaHS) treatment for 2 months elevated H(2)S and NO levels in these mice, and during this period, the D-gal-induced senescent phenotype was reversed. The protective effect of NaHS is associated with a decrease in reactive oxygen species levels and an increase in antioxidants, such as glutathione, and superoxide dismutase and glutathione peroxidase activities. Increased expression of the H(2)S-producing enzymes cystathionine γ-lyase (CSE) and cystathionine-β-synthase (CBS) in the heart, liver, and kidney tissues was observed in the NaHS-treated groups. NaHS supplementation also significantly postponed D-gal-induced HUVEC senescence. Conclusions. Endogenous hydrogen sulphide production in both ageing mice and endothelial cells is insufficient. Exogenous H(2)S can partially rescue ageing-related dysfunction by inducing endogenous H(2)S and NO production and reducing oxidative stress. Restoring endogenous H(2)S production may contribute to healthy ageing, and H(2)S may have antiageing effects.