动物实验,慢性肾功能不全 z-bo 2020-08-22 542

　　Objective: To observe the effect of uremic toxin indoxyl sulfate on aortic atherosclerosis in uremic apoE-/- mice, serum of patients with chronic renal failure, macrophage cholesterol transport receptor expression and intracellular lipid accumulation .

　　Method: Through surgery, the aortic roots of uremic apoE-/- mice, pseudo apoE-/- mice and C57BL/6J mice were used to establish animal models of uremic apoE-/- mice to collect each. Frozen sections were stained with Oil Red O to calculate the relative area of atherosclerotic plaques. Collect the serum of patients with chronic renal failure and normal renal function, and use the serum of patients with chronic renal failure or different concentrations of indoxyl sulfate to intervene the macrophage cell line for 12 hours, and transport cholesterol measurement under different intervention conditions Receptor SR-A1, CD36, ABCA1, ABCG1, SR-B1 mRNA expression; foam cells were induced after 24 hours of intervention, and oil red O staining was used to measure the intracellular lipid content under different intervention conditions.

　　Result: The area of atherosclerotic plaque at the aortic root of uremic apoE-/- mice was significantly larger than that of sham-operated apoE-/- mice. The serum of 5% of patients with chronic renal failure and 250μmol/L indoxyl sulfate can significantly induce the expression of CD36 mRNA in macrophages without affecting the expression of other cholesterol transport receptors.

　　Conclusion: Chronic renal failure accelerates the development of atherosclerosis, and its mechanism is related to the up-regulation of the uremic toxin indoxyl sulfate in the serum of chronic renal failure and the up-regulation of CD36 mRNA expression in macrophages to induce and promote intracellular lipids Quality accumulation.