Effect of nebivolol treatment on atherosclerotic plaque components in apoE-knockout mice.

摘要: INTRODUCTIONApolipoprotein E (ApoE)-knockout mice spontaneouslydevelop atherosclerosis on a chow diet and display extensiveatherosclerotic lesions in major arteries (1). This effect is muchmore pronounced female ApoE-/- which developmarkedly increased aortic compared to males (2).Therefore, they are useful animal model study pathogenesisof investigate the influence of potentialanti-atherogenic drugs (3). The specific inflammatory processleading development atherosclerotic plaque involvesmultiple cell types, including monocyte-derived macrophages,vascular smooth muscle cells (VSMCs), T-lymphocytes, andendothelial cells, as well profound remodeling theextracellular matrix. examination atheroscleroticlesion components provides insight into mechanismsinfluencing formation, stability.Recent studies have demonstrated that nebivolol, thirdgeneration beta1-selective blocker reduces size ofatherosclerotic cholesterol-fed rabbits apoE-deficient (4-6). mechanisms its antiatherogenicaction not clear may include increase vascularnitric oxide release (7), improvement endothelial function (4)and suppression infiltration activationof (8-10). There is, however, very limitedinformation concerning nebivolol thecomposition