Therapeutic efficacy of liraglutide on diabetic nephropathy mice by inhibiting inflammatory factors

Abstract

This study was to investigate the role and mechanism of liraglutide in the treatment of diabetic nephropathy (DN) mice. A mouse model of streptozotocin-induced DN was established. The mice were intraperitoneally injected with liraglutide at a dose of 200 μg/kg for 6 weeks. The expression of interleukin-6 (IL-6), tumor necrosis factor (TNF), and nuclear factor kappa B (NF-κB) messenger RNA (mRNA) in renal tissue of mice was examined by real-time quantitative polymerase chain reaction (PCR). Meanwhile, the expression of IL-6 and TNF protein in renal tissue of mice was detected by western blot, while the expression of NF-κB protein in renal tissues of each group was detected by immunofluorescence. After 6 weeks of intervention, the blood glucose (GLU), total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and weight of the liraglutide group were significantly lower than those of the DN group ( P < 0.01 or P < 0.05), whereas high-density lipoprotein (HDL) was significantly increased ( P < 0.05). At the same time, the microscale albuminuria (MAU) and N-acetyl-β-d-glucosaminidase (NAG) in the liraglutide group were significantly lower than those in the DN group ( P < 0.05). Moreover, the urea (UR), creatinine (CR), and uric acid (UA) in the liraglutide group were significantly lower than those in the DN group ( P < 0.01 or P < 0.05). In addition, the mRNA and proteins of IL-6, TNF, and NF-κB in the liraglutide group were significantly lower than those in the DN group ( P < 0.05). In conclusion, the mechanism of liraglutide in the treatment of DN may be related to the inhibition of the expression of genes and proteins of inflammatory factors.