Objective:To study the role of TOLL-like receptor4/MAPKs pathway of renal tissue in the diabetic rats treated with piogitazone. Methods:The male Sprague Dawlry rats were randomly selected as the control group (n=8) and experimental group(n=32). The experimental rats were randomly divided into three groups. The expression of ERK1/2,JNK and p38MAPK,and levels of their phosphorylation in kidney were measured by Western blot in control group and experimental group. Results:The expression of TOLL-like receptor 4 in all renal tissue in the diabetic rats were significantlyincreased than those in control group (P<0. 01). Compared with the control group. The activity of p-ERK1/2 and p38MAPK significantly increased in each experimental group (P<0. 05),but the expression level of p-JNK was no statistical significance. TOLL-like receptor 4 could regulatory effect on the phorylation of ERK1/2 and p38MAPK. Compared with the model group,the expression of p-ERK1/2 and p38MAPK significantly decreased(P<0. 05),moreover, these changes were more significant in high-dose treated group ( P<0. 05 ) . Conclusion:Pioglitazone inhibits the expression of TOLL-like receptor 4 of renal tissue in the diabetic rats,and these effects may be related to TOLL-like receptor 4/ERK1/2 and TOLL-like receptor 4/p38MAPK pathways.

0.05).In the group with primary common bile duct suture,the occurrence of bile leakage was relative with hyperglycemia(P0.05).Conclusion It is the key factors,including chosing appropriate patients, intraoperative special examination, careful manipulation and effective medical treatment that can reduce the morbidity of bile leakage.

Immunohistocheraistry and RT-PCR were used to examine the expression of toll-like receptor 4 (TLR4) in the kidney of diabetic rats.Compared with normal control group,the expression of TLR4 in diabetes mellitus group was increased ( P ＜ 0.05 ).Compared with diabetes mellitus group,the expression of TLR4 in simvastatin treated group was decreased( P＜0.05 ).The results suggest that TLR4 may play a role in the pathogenesis of diabetic nephropathy.Simvastatin seems to delay the progress of diabetic nephropathy via reducing TLR4 expression.