Pharmacological inhibition of histone deacetylase reduces NADPH oxidase expression, oxidative stress and the progression of atherosclerotic lesions in hypercholesterolemic apolipoprotein E-deficient mice; potential implications for human atherosclerosis.
We investigated the effect of such lipid-lowering interventions on atherosclerosis in APOE*3-Leiden.CETP mice, a well-established model for hyperlipidemia.
Among them, 177 proteins were also differentially expressed in diabetic apolipoprotein E deficient (ApoE-/-STZ) mice, suggesting expression changes associated with atherosclerosis independent of the model used.
Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)-/- mice.
Western blot and fluorescence-activated cell sorting analysis showed that Rheb expression was significantly increased in atherosclerotic lesions of atherosclerosis-prone (apoE<sup>-/-</sup> [apolipoprotein E deficient]) mice fed with Western diet.
For this purpose, 12-week old hyperlipidemic apolipoprotein E knockout mice were fed a Western-type diet for six weeks to induce both hepatic steatosis and atherosclerosis.
44 apolipoprotein E (ApoE)-/- 7 weeks old male rats were randomly divided into normal diet group (NC group) and AS model group (high-fat diet feeding).
In the present study, we used Apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice model and in vitro cell line of RAW264.7 to explore the mechanisms of ethanol extracts of Danlou tablet (EEDT) in treating atherosclerosis.
In this study, we collected blood samples from patients of coronary artery diseases and apolipoprotein E (ApoE)<sup>-/-</sup> mice that were fed a Western diet for 12 wk to induce atherosclerosis and found that serum CTRP13 level was decreased.
The effect of MALAT1 on atherosclerosis was determined in apolipoprotein E-deficient (Apoe<sup>-</sup><sup>/-</sup>) MALAT1-deficient (Malat1<sup>-/-</sup>) mice that were fed with a high-fat diet and by studying the regulation of MALAT1 in human plaques.