In the present study, we found that the expression of α-SMA was significantly decreased, accompanied by increased expression of E-cadherin in TGT-treated DM rats in a dose-dependent matter, but not in untreated DM rats, suggesting that the inhibition of EMT could be an important mechanism by which TGT exerts its effectiveness on renal tubulointerstitial fibrosis. This evidence concerns the gene ACTA1 and diabetes mellitus.