Objective To investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism.Methods In this study, we explored the direct effects of AD on cultured mouse podocytes and the potential protection effects of Dexamethasome (Dex).Results After 24-hour AD (5×10 -7 mol/L) treatment, albumin passage through podocyte monolayers was increased by 2.27-fold (P<0.01). AD caused a 62% decrease in Zonula Occluden -1 (ZO-1) protein (P<0.05), suggesting that AD might increase podocyte permeability by disrupting tight junctions. Dex (1×10 -6 mol/L), co-administered with AD, protected podocytes from AD-induced increased albumin passage. This may be linked with an increased P-cadherin protein level to 1.93 fold of control (P<0.01).Conclusions AD has a direct, detrimental effect on podocyte permeability, probably through disrupting tight junctions; Dex could protect against AD-induced high podocyte permeability by upregulating adherent protein P-cadherin. Objective To investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism. Methods In this study, we explored the direct effects of AD on cultured mouse podocytes and the potential protection effects of Dexamethasome (Dex). Results After 24- (P <0.01). AD caused a 62% decrease in Zonula Occluden-1 (ZO-1) protein (P <0.05), suggesting that AD might increase podocyte permeability by disrupting tight junctions. Dex (1 × 10 -6 mol / L), co-administered with AD, protected podocytes from AD-induced increased albumin passage. This may be linked with an Increased P-cadherin protein level to 1.93 fold of control (P <0.01) .Conclusions AD has a direct, detrimental effect on podocyte permeability, probably through disrupting tight junctions; Dex could protect against AD-induced high podocyte permeability by upregulating adherent protein P -cadh erin.