Objective：To observe the influences of sodium selenite on expression of p38 mitogen-activated protein kinase （p38MAPK） and peroxisome proliferator-activated receptor γ （PPARγ） in rat mesangial cells line HBZY-1, so as to study the role of p38MAPK and PPARγ in diabetic nephropathy and the mechanism by which sodium selenite prevents diabetic nephropathy. Methods： Rat mesangial cell line HBZY-1 was incubated with high glucose, high insulin, H2O2 and advanced glycosylation end products （AGEs） separately before and after HBZY-1 cells were pre-treated with SB203580 （p38MAPK special inhibitor）or sodium selenite. Cells receiving no stimulation were taken as control. The expression of p38MAPK protein and PPARγ mRNA was detected respectively by immunohistochemistry assay and RT-PCR in all groups and the results were compared. Results： High glucose, high insulin, H2O2 and AGEs all activated p38MAPK, increased phospho-p38MAPK expression and decreased the expression of PPARγ mRNA in rat mesangial cells line HBZY-1. The expressions of phospho-p38MAPK protein was markedly inhibited by sodium selenite, while the expression of PPARγ mRNA was significantly increased by SB203580 or sodium selenite in rat mesangial cells lines HBZY-1 （P〈0.01）. Conclusion： p38MAPK may antagonize the expression of PPARγ in rat mesangial cells lines HBZY-1. Sodium selenite, with a similar effect to the agonist of PPARγ,can obviously increase the expression of PPARγ.