Renal damage due to rupture of atherosclerotic plaque of renal artery in ApoE-/- mice / 中华肾脏病杂志

ABSTRACT

Objective To investigate the mechanism of renal damage due to rupture of atheroselerotic plaque of renal artery in apolipoprotein E (ApoE) knock-out mice. Methods The model for atherosclerotie renal artery stenosis (ARAS) was established by using ApoE knockout mice. The model mice with renal artery stenosis <50% were divided into the plaque rupture group and the non-plaque rupture group. Wild-type C57BL/6J mice were used as the control group. All the mice were raised under the same conditions. The renal arteries and kidneys were collected for the following analysis. Nuclear factor-kappa-Bp65 (NF-kBp65), intercellular adhesion molecule 1 (ICAM-1) and P-selectin (P-sel) were determined by Western blotting. The expression of interleukin 6 (IL-6) mRNA was detected by RT-PCR. Immunohistochemistry was performed by using serial sections to detect F4/80-related macrophages. Urine n-acetyl-β-d-glucosaminidase (NAG) activity was determined by direct enzyme-substrate coloration. Results In comparison with the nonplaque rupture group and the control group, the expression of NF-kBp65 protein in the blood, renal artery and kidney increased significantly in the plaque rupture group (P<0.05). The expression of F4/80, ICAM-1, P-sel, and IL-6 mRNA were increased significantly in the plaque rupture group (P<0.05), as compared with the non-plaque rupture group and the control group. The Ser and the activity of urine NAG in the plaque rupture group were higher than those in the non-plaque rapture group. The expression of NF-KBp65 protein differed insignificantly between the control group and the non-plaque rupture group (P>O.05). The group differences in the expression of F4/80, ICAM-1, P-sel, and IL-6 mRNA were similar to those in the expression of NF-KBp65 protein. The group differences in the activity of urine NAG and the Scr were similar to those in the expression of NF-kBp65 protein. Conclusion Rupture of atherosclerotic plaque of renal artery causes renal pathology change and renal function damage, which is mediated by inflammation.