Abstract： Objective To investigate the expression of p38 mitogen actirated protein kinase (p38MAPK) in renal fibrosis in diabetic mice. Methods Male homozygous C57 BL/6 mice were divided at random into control group intraperitoneally(i. p.) injected with citrate buffer and diabetes group received 5 consecutive daily intraperitoneal inserum glucose level exceeding 16.7 mmol/L. Mice were killed at 0,4weeks ,8weeks, 12weeks and 16weeks respectively after STZ injected. The kidney tissues were obtained from diabetic and control mice. Serum glucose, extracellular matrix,and 24 h urinary albumin excretion rate(UAE)and the serum creatinine(Scr) were measured. The kidney tissue was used for histological and morphometric studies of glomerular matrix expansion (PAS), and the expression of phosphorylated p38MAPK and TGFβ1 were measured by immunohisteehemical staining. p38MAPK and TGFβ1mRNA were analyzed by reverse transeriptase-PCR. Results The serum level of glucose in diabetic mice increased significantly. Scr and 24 h UAE, and glomerular matrix expansion in diabetic mice were obviously higher than that in control mice. Phosphorylated p38MAPK and TGFβ1 levels were obviously increased in the kidney of diabetic mice compared with those in control mice(P ＜0. 01) ;TGFβ1 expression was positively related to the expression of phosphorylated p38MAPK. Conclusion The overexpression of phosphorylated p38MAPK in kidney shoud play an important role in the development of renal fibrosis associated with diabetic nephropathy in mice.