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Effect of PPARγ Agonist Rosiglitazone on Stable of Atherosclerotic Plaque

Author: ChenGuoZhu
Tutor: ChenXiaoPing
School: Sichuan University
Course: Department of Cardiology
Keywords: Peroxisome proliferator- activated receptor γ Atherosclerosis Macrophage apoptosis
CLC: R543.5
Type: Master's thesis
Year: 2005
Downloads: 123
Quote: 0
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Abstract


[Objective] : basic and clinical research found that peroxisome proliferator- activated receptor γ (PPARγ) may slow down the development of atherosclerosis (AS) , but the mechanism is unclear . This study was to PPARγ agonist rosiglitazone on macrophage apoptosis in rabbit abdominal aortic atheroma by observing , understanding the role of PPARγ atherosclerotic plaque stability , as well as related mechanisms . [Method ] : 12 weeks of high fat diet male New Zealand long-eared rabbit atherosclerosis model . Randomly divided into experimental and control groups , respectively rosiglitazone and placebo treatment for 4 weeks , to observe the change of rabbit abdominal aortic atherosclerotic plaques , using monoclonal antibodies labeled macrophages the TUNEL staining calculation macrophages the rate of apoptosis and immunohistochemical methods to detect caspase 3 expression in macrophages . [ Results ] : given the high fat diet before and after , and 4 weeks after administration experimental group and a control group of fasting blood glucose did not change significantly . After 4 weeks , the experimental group and the control group , the experimental group was significantly reduced plaque thickness . The total number of CD68 positive cells in the treatment group plaques was 69 ± 11 , lower than the control group, 151 ± 10 ( P lt; 0.05 ) . Macrophage apoptosis was 30.9 ± 1.6%, lower than the control group, 42.4 ± 1.2 % ( P lt; 0.05 ) . Treatment group plaques Caspase3 positive cells 24 ± 5 ??lower than the control group, 46 ± 6

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Vascular disease > Artery disease
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