Apelin‑13 alleviates diabetic nephropathy by enhancing nitric oxide production and suppressing kidney tissue fibrosis.

Diabetes is a serious metabolic disease, and the kidney damage induced by diabetes also seriously affects the survival of patients. Apelin is a molecule that plays a crucial role in lipid metabolism, and recent studies have revealed that apelin‑13, a subtype of apelin, plays an important role in regulating blood glucose levels. However, the role of apelin‑13 in diabetic nephropathy remains unclear. In the present study, a rat model of diabetic nephropathy was constructed by the injection of streptozocin (STZ). During this process, these rats were injected with apelin‑13. The blood glucose, urine protein and insulin levels were determined weekly. Next, the expression of angiotensin domain type 1 receptor‑associated protein (APJ), endothelial nitric oxide synthase (eNOS), E‑cadherin and α‑smooth muscle actin (α‑SMA) in the kidney tissues was determined with western blotting. Then, the endothelial cells of glomerular vessels were cultured with high glucose medium. These cells were treated with apelin‑13 for 24 h. Finally, cell viability of these cells and the expression of APJ, eNOS, E‑cadherin and α‑SMA in these cells were determined with western blotting. As a result, treatment of apelin‑13 induced the lower levels of blood glucose and urine protein. In addition, application of apelin‑13 promoted the production of insulin and alleviated the insulin resistance. Treatment with apelin‑13 promoted the expression of APJ, eNOS and E‑cadherin while it suppressed the expression of α‑SMA in kidney tissues of rats and endothelial cells of glomerular vessels. Furthermore, application of apelin‑13 also promoted the cell viability of these cells. In conclusion, apelin‑13 relieved diabetic nephropathy by promoting the production of nitric oxide (NO) and alleviating the fibrosis of kidney tissues.