Abstract：【Objective】To study the influence of Pam3CysSK4 on renal function of diabetic mice and TLR2 expression of the renal tubular epithelial cells. 【Methods】Twentyfour C57 mice were selected and randomly divided into the normal group, diabetic model group (the model group) and the intervention group, 8 rats in each group. The model group was induced by the use of streptozotocin (STZ) to establish diabetes model in mice. The diabetic mice model was established in the intervention group with intravenous injection of Pam3CysSK4, 100 μg/ week, The normal group mice was given with the same amounts of citrate buffer injection as the other two groups did . After they were fed for 8 weeks,24 h urine and 24 h urine protein were collected and evaluated, mice body and kidney were weighed and calculated , and serum creatinine (Cr), urea nitrogen (BUN), blood glucose and interleukin 1 (IL1) were detected to assess glomerular sclerosis index, and detection was also made on Toll like receptors(TLR2), Nuclear Translocation factor κB (NFκB), myeloiddifferentiationfactor88(MyD88) and monocyte chemotactic protein 1(MCP1) to find out their expression levels.【Results】The blood glucose levels of the intervention group and the model group were higher than that of the normal group. In the intervention group, the kidney weight and kidney weight / body weight were higher than that of the model group, while the model group was higher than the normal group, the difference was statistically significant (P<0.05). Of the intervention group and model group, the Cr, bun, IL1 and 24 h urinary protein content and glomerular sclerosis index ,TLR2, NFκB, MyD88 and MCP1 were higher than those in normal control group, the intervention group were significantly higher than the model group，the differences were statistically significant (P<0.05).【Conclusion】High glucose can increase TLR2 level of mouse renal tubular epithelial cells, activate TLR signaling pathway, promote the release of inflammatory factors and increase the damage to the kidney.
2016, Vol. 33 
