Ezetimibe on rabbit atherosclerosis in rats.docVIP

 PAGE \* MERGEFORMAT 18 Ezetimibe on rabbit atherosclerosis in rats Of: Wang Lihua Zhang Zheying group Lvyun Cheng Zhao Zhao Qi Zeng Ying Zhang satellite navigation [Abstract] Objective ezetimibe on atherosclerosis in rabbits plaques. Methods 24 male New Zealand white rabbits were randomly divided into control group, model group, ezetimibe treatment group, n = 8. fed with normal diet control group, model group were fed high-cholesterol diet (normal diet and high cholesterol diet plus 2% from the preparation of cholesterol), ezetimibe in high-cholesterol diet intervention group by adding 5 mg kg-1 d-1 by folding Mab, continuous feeding 12 w, intimal hyperplasia and the microscope to see the obvious preparation plaque protruding sign of success as a model. HE staining aortic pathological changes, oil red O staining and observation of high performance liquid chromatography aortic smooth muscle cell lipid accumulation conditions, RT PCR detection of aortic smooth muscle cell lipid metabolism-related genes CD36, weekly and Lignans ATP binding cassette transporter A1 (ATP binding cassette transporter A1, ABCA1) mRNA changes; western blot observations membrane ABCA1, protein kinase C @ (protein kinase C @, PKC @) protein expression; PepTag RAssay membrane PKC activity was detected. ezetimibe can result atherosclerotic rabbit intima lesion thinning, lipid reduce plaque accumulation and thus the evolution of reversed; compared to 50 g / ml oxLDL 24 h, the New Zealand rabbit aortic smooth muscle cells, 3 mol / L ezetimibe can effectively reverse the oxLDL-induced foam cell formation, so that intracellular CE / TC ratio fell to 39.6%. ezetimibe significantly reduced smooth muscle cell CD36, perilipin, and the expression of PKC @, increased membrane expression of ABCA1 .3 mol / L ezetimibe reduced aortic smooth muscle cells can be membrane PKC activity to near baseline. Conclusion ezetimibe may be by PKC/CD36 / perilipin / ABCA1 these regulators of lipid accumulat