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LJ-1888, a selective antagonist for A3 adenosine receptor, ameliorates the development of atherosclerosis and hypercholesterolemia in apolipoprotein E knock-out mice
Jong-Gil Park1,#, Se-Jin Jeong2,#, Jinha Yu3, Gyudong Kim3, Lak Shin Jeong3, GOO TAEG Oh4,*
1Biotherapeutics Translational Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB),
2Cardiovascular Division, Department of Medicine, Washington University School of Medicine,
3College of Pharmacy, Seoul National University,
4Immune and Vascular Cell Network Research Center, National Creative Initiatives, Ewha Womans University
Cardiovascular diseases arising from atherosclerosis are the leading causes of worldwide mortality and morbidity. Lipid lowering agents have been developed to treat hypercholesterolemia, a major risk factor for atherosclerosis. However, the prevalence of cardiovascular diseases is increasing, indicating a need to identify novel therapeutic targets and develop new treatment agents. Adenosine receptors (ARs) are emerging as therapeutic targets in asthma, rheumatoid arthritis, cancer, ischemia and inflammatory diseases. This study assessed whether LJ-1888, a selective antagonist for A3 AR, can inhibit the development of atherosclerosis in apolipoprotein E knock-out (ApoE-/-) mice fed a western diet. Plaque formation was significantly lower in ApoE-/- mice administered LJ-1888 than in mice not administered LJ-1888, without liver damage. LJ-1888 treatment of ApoE-/- mice prevented western diet-induced hypercholesterolemia, markedly reducing low-density lipoprotein cholesterol levels and significantly increasing high-density lipoprotein cholesterol concentrations. Reduced hypercholesterolemia in ApoE-/- mice administered LJ-1888 was associated with the enhanced expression of genes involved in bile acid biosynthesis. These findings indicate that LJ-1888, a selective antagonist for A3 AR, may be a novel candidate for the treatment of atherosclerosis and hypercholesterolemia.
Abstract, Accepted Manuscript(in press) [Submitted on April 30, 2018, Accepted on May 21, 2018]
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