科研之友
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摘要
To study the effect of CXCR4 antagonist AMD3100 on the atherosclerotic lesion, the expression of TNF-alpha and NF-kappa B and SDF-1 alpha/CXCR4, so as to approach the specific role and possible mechanisms of SDF-1 alpha/CXCR4 on atherosclerosis. 36 male apoE(-/-) mice, 8 weeks old, randomly divided into three groups: (1) normal food group, (2) high fat group, (3)AMD3100 group. Animals from high fat group and AMD3100 group were fed with western food which including 15% fat and 0.25% cholesterol. After feeding 12 weeks, all mice were anesthetized by 0.2 similar to 0.3 ml Urethane (20%) and removed eyeball in order to obtain blood preparation. Serum lever of SDF-1 alpha was measured by ELISA. Serum triglyceride (TG), total cholesterol (TC), and high density lipoprotein cholesterol (HDL-C) were determined by commercially enzymatic methods. The Hematoxylin/Eosin dyeing of paraffin section was used to detect the area of atherosclerotic plaque of apoE(-/-) mice aortic root transaction. The expression of CXCR4, TNF-alpha and NF-kappa B was analyzed by real time RT-PCR and Western blot, respectively. As a result, AMD3100 treatment resulted in a significant increase of atherosclerotic lesion area and the expression of TNF-alpha and NF-kappa B in apoE(-/-) mice. Serum TG, TC, HDL-C and LDL-C concentrations were not markedly changed. AMD3100 reduced SDF-1 alpha serum lever and CXCR4 expression on artery wall. It can be concluded that, atherosclerotic lesions in apoE(-/-) mice were aggravated by long term administration of CXCR4 antagonist AMD3100. Possible mechanisms of this action for AMD3100 are associated with the up-regulation pro-inflammatory factors TNF-alpha and NF-kappa B and down-regulation SDF-1 alpha/CXCR4 axis.
