Hepatocyte growth factor exerts beneficial effects on mice with type II diabetes‑induced chronic renal failure via the NF‑κB pathway.

Type II diabetes is associated with a low quality of life and inflammation, and is often accompanied by varying degrees of chronic renal failure. Chronic renal failure is considered one of the most important factors that aggravates diabetes and contributes to renal insufficiency in patients with diabetes though cellular fibrosis. It has previously been reported that hepatocyte growth factor (HGF) serves extensive biological roles, and is a multifunctional antifibrotic factor that is involved in kidney development, acute injury and regeneration. The present study aimed to investigate whether HGF exerts beneficial effects on type II diabetes‑induced chronic renal failure in a mouse model. Plasma concentration levels of HGF, tumor necrosis factor (TNF)‑α, monocyte chemoattractant protein (MCP)‑1, interleukin (IL)‑1 and IL‑6 were analyzed prior to and following treatment with HGF. Blood urea nitrogen, plasma creatinine concentrations, and electrolyte, total serum protein, parathyroid hormone and C‑reactive protein levels were analyzed by ELISA. The mechanism underlying the effects of the HGF‑mediated signaling pathway was also investigated in mice with type II diabetes‑induced chronic renal failure. Histological analysis was used to determine the therapeutic effects of HGF on mice with type II diabetes‑induced chronic renal failure. The results indicated that HGF exhibited lower plasma concentrations in mice with type II diabetes‑induced chronic renal failure compared with in healthy mice. In addition, treatment with HGF relieved chronic renal failure via inhibition of inflammation. The results indicated that TNF‑α, MCP‑1 and IL‑1 serum concentration levels were downregulated following treatment with HGF. Conversely, IL‑6 and vascular endothelial growth factor concentration was increased in the HGF‑treated mice compared with in the control mice. The results also demonstrated that HGF treatment downregulated the expression of nuclear factor (NF)‑κB molecules, and target molecules C‑C motif chemokine ligand (Ccl)2, Ccl5, intercellular adhesion molecule 1 and TNF‑α. The present study demonstrated that HGF markedly improved renal failure induced by type II diabetes in a mouse model; histological analyses revealed that renal cell injury was improved following treatment with HGF. In conclusion, these results suggested that HGF may exert beneficial effects on type II diabetes‑induced chronic renal failure via regulation of the NF‑κB signaling pathway.