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Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Biosci 2015 ; 5 (ä): ä Nephropedia Template TP
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Inhibitory effects of Mycoepoxydiene on macrophage foam cell formation and atherosclerosis in ApoE-deficient mice #MMPMID26045945
Xia X; Li Y; Su Q; Huang Z; Shen Y; Li W; Yu C
Cell Biosci 2015[]; 5 (ä): ä PMID26045945show ga
Background: Mycoepoxydiene (MED) is a polyketide that can be isolated from a marine fungus and is associated with various activities, including antitumor and anti-inflammatory functions. However, its effects on atherosclerosis remain unknown. Macrophage-derived foam cells play crucial roles in the initiation and progression of atherosclerotic plaques. In this study, we investigated the effects of MED on oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and activation, and on high fat diet (HFD)-induced atherosclerosis in ApoE-deficient (ApoE?/?) mice. Results: Our findings show that MED could significantly inhibit ox-LDL-induced macrophage foam cell formation and suppress the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), which is a receptor for ox-LDL. Additionally, MED could significantly inhibit the secretion of proinflammatory cytokines, such as tumor necrosis factor (TNF-?), interleukin (IL)-6, and IL-1?. Mechanistically, MED inhibited NF-?B activation by blocking I?B-? degradation and reducing NF-?B DNA binding activity. Moreover, MED dramatically reduced the occurrence of HFD-induced atherosclerotic lesions in ApoE?/? mice. Conclusions: Our study shows that MED can inhibit macrophage foam cell formation and activation by inhibiting NF-?B activation, thereby protecting ApoE?/? mice from HFD-induced atherosclerosis. Our findings suggest that MED might be a potential lead compound for the development of antiatherosclerotic therapeutics. Electronic supplementary material: The online version of this article (doi:10.1186/s13578-015-0017-y) contains supplementary material, which is available to authorized users.