Liraglutide alleviates arteriosclerotic lesions and inhibits receptor for advanced glycation end-product expression in diabetic ApoE-/- mice / 中华内分泌代谢杂志

ABSTRACT

Objective To observe the effect of liraglutide on arteriosclerotic lesions in diabetic ApoE- / - mice via regulating receptor for advanced glycation end-products ( RAGE) expression of aorta. Methods Thirty male ApoE- / - mice (10 weeks) were randomly divided into 3 groups control group, diabetes group, and diabetes +liraglutide group. All the mice were fed a high-fat diet. Diabetes was induced by 2 intraperitoneal injection of streptozotocin (STZ, 55 mg·kg-1 ·d-1 ). Mice were treated with subcutaneous injection of liraglutide (0. 4 mg· kg-1 ·d-1 ) in diabetes+liraglutide group. After 9 weeks, blood was drawn and the aorta were rapidly procured. The serum levels of advanced glycation end-products ( AGEs), soluble receptor for advanced glycation end-products (sRAGE ), stromal cell-derived factor-1α ( SDF-1α ), as well as total cholesterol and triacylglycerol were measured. Atherosclerotic plaque area was determined by Sudan Ⅳ staining. The expression of RAGE was determined using RT-PCR and western blot, respectively. Results Compared with control group, the serum AGEs, the RAGE protein and mRNA expression, the atherosclerotic lesions were significantly increased in the mice of diabetes group. Compared with diabetes group, the serum AGEs, the RAGE protein and mRNA expression, the atherosclerotic lesions were significantly decreased in the mice of diabetes+liraglutide group. Conclusion Liraglutide is confirmed as to have an anti-atherosclerotic effects and inhibits RAGE expression in diabetic ApoE- / - mice.