作者: L. Y. Chau , T. S. Lee , L. J. Wang , R. C. Pai , F. Y. Lee
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摘要: Heme oxygenase-1 (HO-1) is a heme-degradation enzyme induced under various oxidative stress conditions. To elucidate the potential involvement of HO-1 in atherogenesis, expression this atherosclerotic lesions apolipoprotein E-deficient mice and humans were examined. Both immunostaining situ hybridization clearly demonstrated that was prominent endothelium foam cells/macrophages thickened intima from both experimental animals. The also detected medial smooth muscle cells advanced lesions. induction mRNA observed murine peritoneal macrophages after treatment with oxidized low density lipoprotein (LDL) but not native LDL dose-dependent manner. Time course study at 3 hours, reached maximal 6 remained evident up to 24 hours treatment. degree concordant extent oxidation preparation. Lysophosphatidylcholine, one major components present LDL, ineffective induce gene expression, suggesting other lipophilic substances derived are responsible for HO-1. These results demonstrate proteins expressed