Aims. The study was designed to explore whether hydrogen sulphide (H₂S) and nitric oxide (NO) generation changed in D‐galactose‐ (D‐gal‐) induced ageing, the possible effects of exogenous H₂S supplementation, and related mechanisms. Results. In D‐gal‐induced senescent mice, both H₂S 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 H₂S donor (NaHS) treatment for 2 months elevated H₂S 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 H₂S‐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 H₂S can partially rescue ageing‐related dysfunction by inducing endogenous H₂S and NO production and reducing oxidative stress. Restoring endogenous H₂S production may contribute to healthy ageing, and H₂S may have antiageing effects.