JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2016, Vol. 54 ›› Issue (3): 1-4.doi: 10.6040/j.issn.1671-7554.0.2015.1137

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The effect of resistin-like molecule β on the vulnerability of atherosclerotic plaques in ApoE-/- mice

SUN Pengfei, MENG Xiao, ZHANG Kai, LI Li   

  1. The key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China
  • Received:2015-11-20 Online:2016-03-10 Published:2016-03-10

Abstract: Objective To explore the effect of resistin-like molecule β(RELMβ)on the vulnerability of atherosclerotic plaques in ApoE-/- mice. Methods A total of 60 male ApoE-/- mice(8 weeks old)were fed with a high-fat diet and a constrictive silastic tube was placed to induce the vulnerable plaques. All mice were divided into 3 groups after surgery(n=20 per group): control, si-NC and si-RELMβ. At the end of week 14, ApoE-/- mice were euthanized to collect the right common carotid arteries and blood from the left ventricle. The contents of total cholesterol, triglycerides, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol in the blood samples were detected. The protein expressions of RELMβ in all mice were determined with Western blotting. The collagen and lipoid depositions in the plaques were determined with collagen sirius red staining and oil-red O staining, respectively. The contents of macrophages, smooth muscle cells(SMCs), interlenkin-1 beta(IL-1β)and interlenkin-6(IL-6)expressions in the plaques were detected with immunohistochemical methods. Results There were no significant differences in body weight and lipid levels among the 3 groups. Compared with the control group, the si-RELMβ group had significantly decreased RELMβ protein expression, lipid, macrophages, vulnerable index, and expressions of IL-1β and IL-6, increased contents of collagen and SMCs(P<0.05), while those in the si-NC group had no statistical differences. Conclusion RELMβ can increase atherosclerotic plaque instability, and its mechanism is involved with the elevated expressions of IL-1β and IL-6.

Key words: Inflammation, Interlenkin-6, Atherosclerosis, Resistin-like molecule β, Interlenkin-1 beta

CLC Number: 

  • R541.4
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