【摘要】 目的探讨瑞舒伐他汀强化治疗对外周动脉粥样硬化患者细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)的作用及可能机制。方法人选无症状的外周动脉粥样硬化患者20例,服用瑞舒伐他汀5～20 mg/d,治疗3个月,观察患者治疗前后血脂情况及血浆VCAM-1水平;流式细胞学检测单个核细胞ICAM-1表达;实时荧光定量PCR及Western blotting检测单个核细胞过氧化物酶体增殖激活受体γ(PPARγ)的mRNA及核内蛋白表达。结果与基线时比较,瑞舒伐他汀治疗后淋巴细胞表面ICAM-1表达明显降低,单个核细胞核内PPARγ蛋白表达增加。血浆VCAM-1水平、单核细胞表面ICAM-1表达则无明显变化。结论瑞舒伐他汀抑制外周动脉粥样硬化患者单个核细胞ICAM-1的表达,上游机制可能与PPARγ途径有关。更多还原

【Abstract】 Objective To investigate the effect of intensive rosuvastatin therapy on adhesion molecules in patients with peripheral atherosclerosis and explore the possible upstream mechanism.Methods Twenty asymptomatic patients with peripheral atherosclerosis were enrolled and given 5-20 mg/day rosuvastatin for 3 months.Before and after the treatment,the lipid profile and plasma vascular cell adhesion molecule-1(VCAM-1) levels were examined.The expression of intercellular adhesion molecule-1(ICAM-1) in the mononuclear cells was measured using flow cytometry,and the mRNA and protein expressions of peroxisome proliferator-activated receptorγ(PPARγ) were detected using RT-PCR and Western blotting, respectively.Results Compared with the baseline levels,ICAM-1 expression decreased and PPARy protein expression increased in the lymphocyts.Rosuvastatin therapy did not produce obvious effects on plasma VCAM-1 level or ICAM-1 expression in the monocyts in these patients.Conclusion Rosuvastatin produces anti-inflammatory effects by decreasing the expression of ICAM-1 in mononuclear cells,and its upstream mechanism may involve the PPARy pathway.更多还原