Dihydrocapsaicin Attenuates Plaque Formation through a PPARγ/LXRα Pathway in apoE−/− Mice Fed a High-Fat/High-Cholesterol Diet

摘要: Aims Atherosclerosis is a chronic inflammatory disease and represents the major cause of cardiovascular morbidity mortality. There evidence that dihydrocapsaicin (DHC) can exert multiple pharmacological physiological effects. Here, we explored effect DHC in atherosclerotic plaque progression apoE−/− mice fed high-fat/high-cholesterol diet. Methods Results apoE−/− were randomly divided into two groups diet with or without for 12 weeks. We demonstrated cellular cholesterol content was significantly decreased while apoA1-mediated efflux increased following treatment THP-1 macrophage-derived foam cells. also observed plasma levels TG, LDL-C, VLDL-C, IL-1β, IL-6, TNF-α CRP markedly apoA1 HDL-C increased, consistent this, lesion development inhibited by diet. Moreover, both LXRα siRNA PPARγ made up-regulation on ABCA1, ABCG1, ABCG5, SR-B1, NPC1, CD36, LDLR, HMGCR, apoE expression notably abolished down-regulation SRA1 compensated. And DHC-induced had no expression. Conclusion These observations provide direct decrease formation involving PPARγ/LXRα pathway thus may represent promising candidate therapeutic agent prevention atherosclerosis.