Abstract: ObjectiveTo investigate protein expressions of phosphatase and tensin homologue deleted on chromosome 10(PTEN)under high-glucose condition and to explore its role and possible mechanism in rat renal tubule fibrosis pathological changes.MethodsThe rat renal tubular epithelial cells(NRK52E)were cultured in vitro and randomly divided into a normal and a high glucose group.Immunofluorescence cytochemistry staining was used to assess the protein expression of E-cadherin and smooth musle actin-α(α-SMA) and Western blot was used to determinate the PTEN,phosphorylated AKT1(p-Akt1)^(Ser473),E-caderin,and α-SMA protein expression in the cells of different groups at 2,12,24,and 48 hours of the treatment.ResultsCompared with those of the normal glucose group,the protein expressions of PTEN and E-caherin significantly reduced(1.15±0.13,1.10±0.13 and 1.23±0.11,1.22±0.11)(all P<0.05) and the expressions of p-Akt1^(Ser473) and α-SMA increased remarkably(1.53±0.13,1.60±0.13 and 1.86±0.10, 1.91±0.10)(all P<0.05)in high glucose group at 24 and 48 hours of the treatment.The expression of PTEN was positively correlated with E-cadherin protein(P<0.05)and negatively correlated with α-SMA expression(P<0.05).ConclusionThe expression of PTEN protein significantly reduced in rat renal tubular epithelial cells 24 and 48 hours after high-glucose treatment and the decrease may facilitate the initiation and development of renal tubule fibrosis by alleviating the inhibitory effect through PI3K/Akt signal pathway.