Objective: To investigate the therapeutic effect and mechanism of Triptolide on renal injury in diabetic nephropathy rats.
Methods: A total of 15 male SD rats aged 8 weeks were randomly divided into five groups (3 rats in each group): control
group, model group, Triptolide low-dose (Triptolide-L) group, Triptolide medium-dose (Triptolide-M) group, Triptolide
high-dose (Triptolide-H) group. The rats models of diabetic nephropathy (DN) were established by a single intraperitoneal
injection of STZ after being fed with high-fat and high-sugar diet for 4 weeks, and the fasting blood glucose (FBG) concentration of rats was detected. After 4 weeks, HE-staining was used to evaluate the renal pathological damage in rats; biochemical analysis was used to determine the blood urea nitrogen (BUN), serum creatinine (SCr), total cholesterol (TC), triglyceride (TG); ELISA was used to measure the serum inflammatory factor levels; Western blot (WB) was used to detect
the expression of TGF-β1/Smads pathway proteins.
Results: In the four FBG tests (once a week), the FBG concentration in the model group was significantly higher than that in
the control group, while Triptolide-treated rats were significantly lower than that in the model group. Rats in Model group
showed obvious renal injury, and Triptolide significantly improved the renal injury in DN rats. Compared with the control
group, the expression of BUN, SCr, TC, TG, inflammatory factors TNF-α, IL-6 and IL-1β in the model group increased significantly. WB results showed that the expressions of TGF-β1, Smad3, α-SMA and vimentin in the kidney significantly increased, while the Smad7 expression significantly decreased. Triptolide significantly reduced the levels of BUN, SCr, TC,
TG and TNF-α, IL-6, IL-1β in diabetic rats, decreased the expression of TGF-β1, Smad3, α-SMA, vimentin, and increased
the Smad7 expression. In different doses of Triptolide treatment group, its effect showed a significant concentration dependence.
Conclusion: Triptolide alleviates renal injury in diabetic rats by inhibiting the TGF-β1/Smads signaling pathway.