To investigate the protective mechanism of cinnamon polyphenols(CPS) against kidney injury in diabetic rats，with a focus on the inhibition of renal NOD-like receptor family pyrin domain-containing 3(NLRP3).Methods:A diabetic rat model was established via a high-fat diet combined with intraperitoneal injection of streptozotocin(STZ).Diabetic rats were treated with irbesartan(27 mg/kg)，and high-，medium-，and low-dose CPS(200，100，and 50 mg/kg)，with continuous administration for 8 weeks.After treatment，fasting blood glucose(FBG)，total cholesterol(TC)，triglycerides(TG)，microalbuminuria(MAU)，glycated serum protein(GSP)，and kidney index(KI) were measured.Renal histopathological changes were assessed by periodic acid-Schiff(PAS) and periodic acid-silver methenamine(PASM) staining.Serum interleukin-1β(IL-1β) levels were detected by enzyme-linked immunosorbent assay(ELISA)，and the protein expression of NLRP3，caspase-1，and IL-1β was analyzed by Western blot.Results:Compared with the normal group，the model group exhibited significantly increased levels of FBG，GSP，KI，MAU，serum IL-1β，and renal NLRP3，caspase-1，and IL-1β protein expression(P<0.01 or P<0.05)，accompanied by aggravated renal pathological damage.CPS treatment significantly reduced FBG(P<0.01)，KI(P<0.05)，MAU，TC，TG(P<0.01)，and GSP(P<0.05) levels.Additionally，CPS downregulated serum IL-1β and renal cortical expression of NLRP3，caspase-1，and IL-1β protein expression(P<0.05)，and alleviated tubular epithelial cell injury.Conclusion:CPS alleviates renal inflammation in diabetic rats by inhibiting NLRP3 activation and NLRP3-mediated IL-1β maturation，thereby exerting a protective effect against diabetic nephropathy