动物造模,糖尿病 z-bio 2023-05-11 910

　　Objective: To investigate the effect of TAK1 inhibitor on MAPK and NF-κB signaling pathways in diabetic rats and its protective mechanism on kidneys.

　　METHODS: Forty-eight rats were divided into DN group, TAK1 group and control group according to the random number table method, with 16 rats in each group. The rats in the control group were fed normally without any treatment; the rats in the DN group and the TAK1 group were given intraperitoneal injection of 1% 50 mg/kg STZ to establish the DN rat model. Eight rats in each group were sacrificed at 4 weeks and 8 weeks, respectively, and the pathological changes of renal tissue of the rats in each group were observed, and the expressions of serum TNF-α, MCP-1, and IL-1β, and the protein expressions of p38MAPK and NF-κBp63 in renal tissue were detected. And p38MAPK, NF-κBp63 mRNA expression.

　　Results: At 4 weeks and 8 weeks, the body weight, blood sugar and UAER of the DN group and TAK1 group were significantly higher than those of the control group (P<0.05), and the body weight and UAER of the DN group were significantly higher than those of the TAK1 group (P<0.05). 0.05). The serum levels of TNF-α, MCP-1 and IL-1β in the DN group and TAK1 group were significantly higher than those in the control group (P<0.05), and the above indexes in the DN group were higher than those in the TAK1 group (P<0.05). The expression levels of p38MAPK, NF-κBp63 protein and mRNA were significantly higher than those in the control group (P<0.05), and the above indexes in the DN group were higher than those in the TAK1 group (P<0.05).

　　Conclusion: TAK1 induces inflammatory response by activating MAPK and NF-κB signaling pathway, and participates in diabetic kidney injury; TAK1 inhibitor can down-regulate the expression and release of inflammatory factors and play an anti-inflammatory effect.