Objective: To investigate the effect of TAK1 inhibitor on MAPK and NF-κB signaling pathways in diabetic rats and its protective effect on the kidneys.
Method: Using 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 did not do any feeding and were injected intraperitoneally with 1% 50 mg/kg STZ to the DN and TAK1 groups to establish a DN rat model. At the 4th and 8th week, 8 rats in each group were sacrificed to observe the pathological changes of the kidney tissues of each group and observe the expression of serum TNF-α, MCP-1, IL-1β and p38MAPK in the kidney tissues. And detect the expression of NF-κBp63 protein. And express p38MAPK, NF-κBp63 mRNA.
Results: In the 4th and 8th weeks, the body weight, blood glucose and UAER of the DN group and the TAK1 group were significantly higher than those of the control group (P\u003c0.05). The body weight and UAER of the DN group were significantly higher than those of the TAK1 group. (P\u003c0.05). The levels of serum TNF-α, MCP-1 and IL-1β in the DN and TAK1 groups were significantly higher than those in the control group (P \u003cu\→ u\→ u\→ u\→ c0.05), while the above indicators of the DN group rats Is TAK1 \u003cp \u003c0.01\→(P \u003cu\→ u \u003cu\→ c \u003c0.05). \u003c0.05); The expression levels of p38MAPK, NF-κBp63 protein and mRNA in the DN and TAK1 groups were significantly higher than those in the control group (P\u003c0.05) and higher than those in the DN group. This index is higher than the TAK1 group (P\u003c0.05).
Conclusion: TAK1 induces inflammation and participates in diabetic nephropathy by activating MAPK and NF-κB signaling pathways; TAK1 inhibitors inhibit the expression and release of inflammatory factors, and it has anti-inflammatory effects.