机构地区:[1]Department of Cardiology, the First People's Hospital, Shanghai Jiaotong University [2]Shanghai Institute of Hypertension, School of Medicine, Shanghai Jiaotong University
出 处:《Journal of Shanghai Second Medical University(Foreign Language Edition)》2008年第2期135-140,共6页上海第二医科大学学报(英文版)
摘 要:Objective To determine whether pravastatin exerts anti-oxidative effects on preventing aortic" atherosclerosis via modulating p38 MAPK pathway. Methods Male 8-week-old apoE^-/- mice fed a diet containing 1.25% cholesterol (wt/wt) were divided into pravastatin group administered with pravastatin (80 mg. kg ^-1· d^-1 ) and atherosclerosis group administered with PBS; and male 8-week-old C57BL/6J mice fed a normal diet were as control group ( n = 12 ). In thoracoabdominal aortas of mice, levels of Malondialdehyde ( MDA ) and activities of superoxide dismutase ( SOD ) were measured and expression of phosphorylated p38 MAPK ( p-p38 MAPK) and phosphorylated signal transducer and activator of transcr(ption 1 (pSTAT1) were examined by Western blotting. Results After eight weeks, atherosclerosis in aortic root was significantly prevented by pravastatin. In aortic atherosclerosis lesion, the level of MDA was significantly reduced; adversely the activity, of SOD was increased. Expressions of p-p38 MAPK and pSTAT1 were significantly decreased in aortic atherosclerosis lesion. Conclusion Our results suggests that anti-oxidative mechanisms of pravastatin preventing aortic atherosclerosis may partially depend on modulating p38 MAPK signal pathway.Objective To determine whether pravastatin exerts anti-oxidative effects on preventing aortic atherosclerosis via modulating p38 MAPK pathway. Methods Male 8-week-old apoE-/- mice fed a diet containing 1.25% cholesterol (wt/wt) were divided into pravastatin group administered with pravastatin (80 mg·kg-1·d-1) and atherosclerosis group administered with PBS; and male 8-week-old C57BL/6J mice fed a normal diet were as control group (n=12). In thoracoabdominal aortas of mice, levels of Malondialdehyde (MDA) and activities of superoxide dismutase (SOD) were measured and expression of phosphorylated p38 MAPK (p-p38 MAPK) and phosphorylated signal transducer and activator of transcription 1 (pSTAT1) were examined by Western blotting. Results After eight weeks, atherosclerosis in aortic root was significantly prevented by pravastatin. In aortic atherosclerosis lesion, the level of MDA was significantly reduced; adversely the activity of SOD was increased. Expressions of p-p38 MAPK and pSTAT1 were significantly decreased in aortic atherosclerosis lesion.Conclusion Our results suggests that anti-oxidative mechanisms of pravastatin preventing aortic atherosclerosis may partially depend on modulating p38 MAPK signal pathway.
关 键 词:pravastatin atherosclerosis p38 MAPK signal pathway
分 类 号:R543.12[医药卫生—心血管疾病]
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