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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.
Objective To determine whether pravastatin exerts anti-oxidative effects on preventing aortic atherosclerosis via modulating the 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 been 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 pSTAT 1 were significantly decreased in aortic atherosclerosis lesion.Conclusion Our results suggests that anti-oxidative mechanisms of pravastatin preventing aortic atherosclerosis may partially dependent on modulating p38 MAPK signal pathway.