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.
ABSTRACT
Aim To observe the effects of the total fla-vonoids of scutellaria barbataon ( TFSB ) on high-fat feeding ApoE gene deficiency mice in early atheroscle-rosis ( AS ) and its underlying mechanisms. Methods 40 ApoE-/ -male mice were divided into five groups:model group, SIM group and L-TFSB, M-TFSB, H-TFSB group, 5 C57BL/6J mice were selected as nor-mal control group. All mice in experimental group were fed with high-lipid diet for 4 weeks and all mice were killed after 8 weeks. H&E staining was used to observe morphology of aorta. Blood rheometer was used to ex-amine plasm viscosity and whole blood viscosity. Fully automatic biochemical analyser was used to detect the serum levels of TG, TC, LDL-C and HDL-C. The ex-pression levels of PLTP and VE in serum were meas-ured by ELISA. The expression levels of PLTP and FXR in liver were examined by Western blot. Results The model was established successfully. TFSB groups could improve the aorta AS morphology of model mice and significantly reduce the serum levels of TG, TC and LDL-C, while increase the level of HDL-C ( P hematocrit value, plasma viscosity and whole blood vis-cosity of AS model mice significantly and had statistical significance when compared with model group ( P <0. 01 ) . The expression levels of PLTP of serum were reduced significantly when compared with model group ( P <0. 01 ) . We also found that the expression of PLTP was in negative correlation with VE ( r = -0. 675,P<0. 01). M-TFSB and H-TFSB group could decrease the expressions of PLTP and FXR of liver when compared with model group ( P <0. 01 ) . Con-clusion TFSB may exert its anti-AS effect partly through inhibiting the levels of FXR and PLTP of ApoE-/ -mice, increasing the level of VE, regulating blood lipids, improving blood rheology and reducing the damage of AS in mice.