Hydrogen sulfide exhibits cardioprotective effects by decreasing endoplasmic reticulum stress in a diabetic cardiomyopathy rat model.

Endoplasmic reticulum (ER) stress is critical in the occurrence and development of diabetic cardiomyopathy (DC). Hydrogen sulfide (H2S) has been found to be the third gaseous signaling molecule with anti‑ER stress effects. Previous studies have shown that H2S acts as a potent inhibitor of fibrosis in the heart of diabetic rats. This study aimed to demonstrate whether H2S exhibits protective effects on the myocardium of streptozotocin (STZ)‑induced diabetic rats by suppressing ER stress. In this study, diabetic models were established by intraperitoneal (i.p.) injection of 40 mg/kg STZ. The STZ‑treated mice were divided into three groups, and subsequently treated with normal saline, 30 µmol/kg or 100 µmol/kg NaHS, i.p., respectively, for 8 weeks. The extent of myocyte hypertrophy was measured using hematoxylin and eosin‑stained sections and collagen components were investigated using immunostaining. The expression of glucose-regulated protein (Grp78), C/EBP‑homologous protein (CHOP) and caspase‑12 in the heart tissue of each group was detected by western blot analysis. It was demonstrated that H2S could improve myocardial hypertrophy and myocardial collagen deposition in diabetic rats. In addition, it could reduce the expression of Grp78, caspase-12 and CHOP. In conclusion, these findings demonstrate that H2S suppresses STZ‑induced ER stress in the hearts of rats, and it may serve as a novel cardioprotective agent for DC.