Abstract
The aim of the present study was to investigate the effects of urantide on the expression status of C-reactive protein (CRP) and the inflammatory cytokines monocyte chemotactic protein (MCP)-1 and transforming growth factor (TGF)-β in the aortas of rats with atherosclerosis (AS), and to identify its underlying mechanisms. The effects of urantide in a rat model of AS and in cultured rat vascular smooth muscle cells (VSMCs) were analyzed via hematoxylin and eosin staining, immunohistochemical staining and ELISA. The results in vivo demonstrated that urantide downregulated the expression of inflammatory mediators CRP and MCP-1 and upregulated the expression of TGF-β. The results in vitro indicated that urantide inhibited the proliferation of VSMCs. In addition, urantide reduced the expression of CRP and downregulated the secretion of TGF-β in the culture supernatant. In conclusion, urantide ameliorated the arterial inflammatory damage that was observed in the AS rat model at the cell and tissue levels by controlling the expression of CRP and the inflammatory cytokines MCP-1 and TGF-β. Therefore, urantide may be a potential agent for the complementary treatment of AS.
Highlights
Atherosclerosis (AS) is a common cardiovascular disease and a predominant cause of human fatalities [1]; its mechanism and methods of treatment are an interesting field within medical research
Fetal bovine serum (FBS) was purchased from Tianjin Haoyang Biological Manufacture Co., Ltd. (Tianjin, China), anti-α‐smooth muscle actin (SMA) monoclonal antibody was purchased from Beijing Biosynthesis Biotech Co., Ltd. (Beijing, China) and anti-rat C‐reactive protein (CRP), Monocyte chemotactic protein (MCP)-1 and Transforming growth factor (TGF)‐β monoclonal antibodies were purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA)
Urantide is an antagonist of the Urotensin II (UII) receptor, G protein‐coupled receptor 14 (GPR14), which is able to competitively bind to GPR14, antagonizing aortal contraction in rats [12,13]
Summary
Atherosclerosis (AS) is a common cardiovascular disease and a predominant cause of human fatalities [1]; its mechanism and methods of treatment are an interesting field within medical research. The balance between pro‐ and anti‐inflammatory cytokines is the key factor that determines the occurrence of AS [8,9,10,11]; the investigation of inflammation‐associated molecules is significant to the treatment of AS
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