关键词: 血管内皮炎症, 己糖胺生物合成通路, 细胞间黏附分子-1, 血管细胞黏附分子-1, 6-重氮-5-氧代-L-正亮氨酸

Abstract: Background　Atherosclerosis (AS) is the main pathological basis of cardiovascular disease，which is characterized by vascular endothelial inflammation. Therefore，targeting inflammation related mechanisms is the key to prevention and treatment of AS. Objective　To investigate the effect of the hexosamine biosynthesis pathway (HBP) on adhesion molecules and its regulatory role in vascular endothelial inflammation. Methods　24 SPF grade C57BL/6 female mice were randomly divided into 4 groups：control group，DON group，HFD group，HFD+DON group. Serum and aortic tissue of the mice were collected after high fat diet and intraperitoneal injection of DON for 15 weeks. Serum lipid levels of mice before and after intervention were detected by biochemical kit，pathological changes of aortic root were detected by HE staining，and expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were detected by immunofluorescence staining，ELISA and Western blot. Results　After 15 weeks of intervention，compared with the control group，the levels of LDL-C and TC in the HFD group were significantly increased，while HDL-C was significantly reduced (P<0.05). There was no change in blood lipid levels between the HFD group and HFD+DON group. HE staining results showed that the vascular intima in HFD group was thickened，the vascular smooth muscle was abnormal in shape，the structure was disordered，and a large number of foam cells could be seen. The myocardial cells in HFD+DON group were arranged neatly，the number of foam cells was significantly reduced，the arrangement of endometrial cells was restored，and the cell gap was basically normal. The results of immunofluorescence staining，ELISA and Western blot showed that the expression of ICAM-1 and VCAM-1 in HFD+DON group was down-regulated compared with that in HFD+DON group. Conclusion　Inhibition of HBP can down-regulate the expression of adhesion molecules ICAM-1 and VCAM-1，and play a role in improving vascular endothelial inflammation.

Key words: Vascular endothelial inflammation, Hexosamine biosynthetic pathway, Intercellular adhesion molecule-1, Vascular cell adhesion molecule-1, 6-diazo-5-oxo-L-norleucine