Advanced glycosylation end products increase cellular inflammation in atherosclerotic plaques / 中华肾脏病杂志

ABSTRACT

Objective To test the hypothesis that advanced glycosylation end products(AGEs) increase cellular inflammation in atherosclerotic plaques. Methods Fifty rabbits were randomly divided into five groups. Hypercholesterolemic (0.5% cholesterol in diet) rabbits received repeated intravenous injection of either AGEs modified rabbit serum albumin (AGEs-RSA ) (group A) or unmodified RSA (group B) for 10 weeks. Rabbits treated with either hypercholesterolemic diet (group C)or with a normal diet(group D) or with a normal diet, and intravenous injection of AGEs-RSA (group E) were served as controls. Aortas were harvested at the 10th week, and lipid deposition was quantitated by oil red 0 staining. Macrophage (RAM-11 positive cells) and T lymphocyte (CD43 positive cells) infiltration, smooth muscle cell(?-actin positive cells) migration and proliferation were determined by using immunohistochemical staining and image-analysis techniques. Results Atherosclerotic plaques could be found in animals fed with hypercholesterolemic diet.Lipid deposition in plaque was significantly higher in group A (71.86%?8.3%) than those in group B (53.76%?3.72%)and group C (56.67%?9.2%). Infiltrations of macrophage[ (23.1?8.5)/0.01 mm2]and T lymphocyte[ (15.1 ? 3.8)/0.01 mm2]as well as migration and proliferation of smooth muscle cell [ (19.2?5.7)/0,01 mm2] in atherosclerotic lesions were significantly increased in animals treated with hypercholesterolemic diet and received injection of AGEs-RSA (group A) when compared with group B [macrophage (14.4? 5.9)70.01 mm2; T lymphocyte (9.1?2.6)/0.01 mm2; smooth muscle cell (12.9?3.8)/0.01 mm2]and group C[macrophage (15.4?4.4)/0.01 mm2; T lymphocyte (10.5?2.2)/0.01 mm2, smooth muscle cell (13.8?3.9)/0.01 mm2]. Neither plaque nor a cellular inflammation was found in animals fed with normal diet (group D)and in those received repeated injections of AGEs-RSA (group E). Conclusion AGEs increase cellular inflammation in atherosclerotic plaques and may accelerate formation of atherosclerosis in AGEs associated diseases.