Effect of Dalteparin on Atherosclerotic Lesion Formation in Apolipoprotein E-Deficient Mice. (April 2015)

• Record Type: Journal Article
• Authors: Su, Lin; Zhang, Qingwen; Bao, Hui; Li, Wei; Miao, Yide; Yan, Zheng; Chen, Dingbao
• Is Part Of: Clinical and applied thrombosis/hemostasis. Volume 21:Number 3(2015:Apr.)
• Page Start: 266
• Page End: 272
• Publication Date: 2015-04
• Subjects: atherosclerosis -- dalteparin -- lectin-like oxidized LDL receptor 1; Hemostasis -- Periodicals; Thrombosis -- Periodicals; 616.13
• DOI: 10.1177/1076029613499818
• Languages: English
• ISSNs: 1076-0296

Abstract

We aimed to investigate whether prolonged treatment with dalteparin could inhibit plaque progression. With C57BL/6J mice as the control, genetically deficient apolipoprotein E (apo E) male mice of C57BL/6J strain (apo E −/− ) were randomly divided into 3 groups. The model group received no dalteparin, while the other 2 groups received dalteparin at 100 and 200 U/kg d, respectively. The aorta was harvested for hematoxylin and eosin staining to observe plaque formation and for immunohistochemical staining to detect the expression of oxidized low-density lipoprotein receptor 1 (LOX-1). The expression of LOX-1 messenger RNA was detected by reverse transcription polymerase chain reaction, while the expression of LOX-1 protein was detected by Western blotting. Dalteparin decreased aortic plaque volume and inhibited aortic LOX-1 protein expression in apo E −/− mice. The effect persisted 4 weeks after dalteparin treatment was discontinued. Dalteparin may inhibit atherosclerotic lesions by downregulating the expression of LOX-1 protein.