ABSTRACT
AIM:To explore the effect of CXCL16 deficiency on streptozocin ( STZ)-induced diabetic nephrop-athy in mice.METHODS:CXCL16 knockout ( C16 KO) mice (8 years old) were used to build up diabetes model by treating with STZ.Age-and gender-matched wild-type ( WT) C57BL/6J mice treated with STZ were used as control.All mice were fed with chow diets for 12 weeks, and the development of diabetic nephropathy was evaluated.RESULTS:Compared with the WT mice treated with STZ, C16 KO mice treated with STZ presented lower fasting glucose levels and better glucose tolerance power.C16 KO mice treated with STZ also had lower urine protein levels and smaller areas of glo-merular injury as compared with WT mice treated with STZ.Furthermore, CXCL16 deficiency decreased the contents of re-nal reactive oxygen species ( ROS) , malondialdehyde ( MDA) and oxidized low-density lipoprotein ( ox-LDL) and the mR-NA expression of lectin-like oxidized low-density lipoprotein receptor 1 (Lox-1), and attenuated the expression of renal in-flammatory factors including tumor necrosis factor α( TNF-α) and interleukin 6 ( IL-6) , as well as chemokines including intercellular cell adhesion molecular 1 (ICAM-1) and chemokine C-X-C motif ligand 1 (CXCL1).CONCLUSION:CX-CL16 deficiency obviously inhibits the development of STZ-induced diabetic nephropathy in mice.