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- W2906486319 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." @default.
- W2906486319 created "2019-01-01" @default.
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- W2906486319 date "2018-01-01" @default.
- W2906486319 modified "2023-09-26" @default.
- W2906486319 title "Therapeutic efficacy of liraglutide on diabetic nephropathy mice by inhibiting inflammatory factors" @default.
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- W2906486319 doi "https://doi.org/10.1177/2058739218819283" @default.
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