Puerarin improving renal injury of diabetic mice by regulating TLR4-MyD88-NF-κB signaling pathway

Objective: To investigate the effect of puerarin on renal injury of diabetic mice by regulating TLR4-MyD88-NF-κB signaling pathway. Methods: The diabetic mouse models were established by intraperitoneal injection of streptozotocin(STZ), and were divided into diabetic model group(model group), metformin group as well as puerarin group, and a normal control group was set up. The normal control group and model group were administrated with normal saline, the metformin group was administrated with metformin 320 mg/kg·d^-1, the puerarin group was intervened with puerarin 65 mg/kg·d^-1 intraperitoneally, and all experimental groups were treated for 4 weeks. The fasting blood glucose (FBG) and the weight of the mice in each group were measured weekly. Serum creatinine(Scr), interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) of the mice were determined by enzyme-linked immunosorbent assay (ELISA). The pathological changes of renal tissue were observed by hematoxylin and eosin(HE) staining. The expression levels of Toll-like receptor-4(TLR4), myeloid differentiation factor 88(MyD88) and nuclear factor κB(NF-κB) in renal tissue were observed by immunohistochemistry. Results: Compared with the normal control group, the levels of FBG, Scr, IL-6 and TNF-α in the model group were significantly increased(P＜0.05),the glomeruli was enlarged, the normal renal tissue structure was destroyed, the basement membrane of glomeruli was thickened, and the expression of TLR4, MyD88 and NF-κB protein in renal tissue was increased(P＜0.05).Compared with the model group, the contents of FBG, Scr, IL-6 and TNF-α the in the puerarin group were significantly decreased(P＜0.05), the renal tissue injury was alleviated, and the expression of TLR4, MyD88 and NF-κB in renal tissue was reduced(P＜0.05). Conclusion: Puerarin can significantly improve renal injury of diabetic mice, which may be related to the regulation of TLR4-MyD88-NF-κB signaling pathway.