Objective      To investigate the role of calcitriol on advanced glycation end products (AGEs) induced epithelial-mesenchymal transition (EMT) in renal tubular epithelial cells and explore the possible mechanism.       Methods      NRK52E cells were pretreated with calcitriol and divided into 4 groups upon the addition of AGEs

i.e.

control group

AGEs group

AGEs groups pretreated with low (10 nmol/L) and high (100 nmol/L) concentration of calcitriol. The expression of E-cadherin

alpha smooth muscle actin (α-SMA)

receptor for AGE (RAGE) and phosphorylation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were measured by Western blotting and reverse real-time quantitative polymerase chain reaction (RT-PCR).       Results      Calcitriol alone had no obvious effect on the expression of E-cadherin and α-SMA in rat renal tubular epithelial cells. AGEs down-regulated E-cadherin and up-regulated α-SMA in comparison to the control. AGEs also enhanced the expression of RAGE and phosphorylation of NF-κB. Calcitriol could significantly reverse all the aforementioned effects induced by AGEs (P0.05). When treated with anti-RAGE antibody AF1616

AGEs-induced reduction in E-cadherin and increase in α-SMA were inhibited. Furthermore

NF-κB inhibitor IMD0354 partly attenuated AGEs-induced up-regulation of RAGE via inhibition of calcitriol.       Conclusion      Mechanistically

calcitriol suppresses EMT in renal tubular epithelial cells through downregulation of RAGE and blockage of NF-κB phosphorylation.