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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。
Objective To investigate the effect of rosuvastatin on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in patients with peripheral atherosclerosis and its possible mechanism. Methods Twenty patients with asymptomatic peripheral atherosclerosis were treated with rosuvastatin 5 ~ 20 mg / d for 3 months. The levels of lipids and plasma VCAM-1 levels were observed before and after treatment. Flow cytometry The expression of ICAM-1 was detected by real-time fluorescent quantitative PCR and Western blotting. The mRNA and protein expression of peroxisome proliferator-activated receptor γ (PPARγ) in mononuclear cells were detected by real-time fluorescence quantitative PCR and Western blotting. Results Compared with baseline, the expression of ICAM-1 on the surface of lymphocytes was significantly decreased after rosuvastatin treatment, and the expression of PPARγ protein in nucleus of mononuclear cells increased. Plasma VCAM-1 levels, monocyte surface expression of ICAM-1 no significant change. Conclusion Rosuvastatin inhibits the expression of ICAM-1 in peripheral blood mononuclear cells in peripheral artery atherosclerosis. The upstream mechanism may be related to the PPARγ pathway.