OBJECTIVE： To investigate the effect of Cyslosorus acuminatus flavonone glycoside （CAF） on kidney epithelial-mesenchymal transition （EMT） in rats with diabetic kidney disease （DKD）. METHODS： Rats were randomly divided into normal group （normal saline）， model group （normal saline）， positive group [rosiglitazone， 0.4 mg/（kg·d）]， CAF high-dose and low- dose groups [12.5， 25 mg/（kg·d）]， 10 in each group. Except for normal group， other groups were intraperitoneally injected streptozotocin （60 mg/kg）+high fat diet to induce DKD， and intragastrically administrated related medicines in 13-16 weeks. After the experimental period， fasting blood glucose level and serum creatinine （Scr）， blood urea nitrogen （BUN） contents of rats were detected， collagen deposition and basement membrane thickening in kidney tissue were observed. Immunohistochemistry was used to detect α-smooth muscle actin （α-SMA）， fibronectin， epithelial cadherin （E-cadherin） expressions in kidney tissue， and Western blot was used to determine the glycogen synthase kinase 3β （GSK-3β）， phosphorylated GSK-3β （p-GSK-3β）， β-catenin expressions in kidney tissue. RESULTS： Compared with normal group， fasting blood glucose level， Scr and BUN contents in model group were significantly increased （P＜0.01）； kidney tissue showed obvious collagen deposition and basement membrane thickening；the α-SMA， fibronectin， β-catenin expression levels and GSK-3β phosphorylation degree in kidney tissue were significantly increased （P＜0.01）， while E-cadherin expression levels was significantly decreased （P＜0.01）. Compared with model group， fasting blood glucose level， Scr and BUN contents in each administration group were significantly reduced （P＜0.05 or P＜0.01）；collagen deposition and basement membrane thickening in kidney tissue were significantly improved；the α-SMA， fibronectin， and β-catenin expression levels and GSK-3β phosphorylation degree in kidney tissue were significantly decreased （P＜0.05 or P＜0.01），while E-cadherin expression levels in positive group and CAF high-dose group were significantly increased （P＜0.01）. CONCLUSIONS： CAF can inhibit the kidney EMT of rats with DKD， the molecular mechanism may be associated with downregulating β-catenin expression and inhibiting GSK-3β phosphorylation inactivation.