动物造模,糖尿病 z-bio 2022-01-13 523

　　Objective: To discuss the effect of TAK1 inhibitor on MAPK and NF-κB signaling pathways in diabetic rats and its mechanism of kidney maintenance.

　　Method: According to the random number table method, 48 rats were divided into DN group, TAK1 group and control group, 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 TAK1 group were injected intraperitoneally with 1% 50 mg/kg STZ to establish a DN rat model. Eight rats in each group were sacrificed at 4 weeks and 8 weeks respectively. The pathological changes in the kidney tissue of each group were observed, and the expression of serum TNF-α, MCP-1, IL-1β, and the protein expression of p38MAPK and NF-κBp63 in kidney tissue were detected. And p38MAPK, NF-κBp63 mRNA expression.

　　Results: At 4 weeks and 8 weeks, the body mass, blood glucose and UAER of the DN group and TAK1 group were significantly higher than those of the control group (P<0.05). The body mass and UAER of the DN group were significantly higher than those of the TAK1 group (P<0.05). 0.05). The levels of serum 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). The above indicators of rats in the DN group were higher than those in the TAK1 group (P<0.05); DN group and TAK1 group The expression levels of p38MAPK, NF-κBp63 protein and mRNA were significantly higher than those of 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 through activation of MAPK and NF-κB signaling pathways, and participates in diabetic kidney damage; TAK1 inhibitors can down-regulate the expression and release of inflammatory factors to exert anti-inflammatory effects.