中文摘要：

目的：探讨瑞舒伐他汀对颈动脉粥样硬化患者单个核细胞CC类趋化因子受体2（CCR2）表达的影响及上游机制。方法：选择颈动脉粥样硬化患者20例。予瑞舒伐他汀5~20 mg/d治疗。在基线、3月时采集血标本,测定单核细胞趋化蛋白-1（MCP-1）及血脂水平;分离单个核细胞,流式细胞学检测单个核细胞上的CCR2表达;荧光定量逆转录PCR法检测CCR2、过氧化物酶体增生物激活受体（PPAR）βm RNA的表达;Western印迹法检测PPARβ蛋白的表达。结果：瑞舒伐他汀治疗3个月后,患者低密度脂蛋白胆固醇（LDL-C）水平明显降低（P〈0.01）,MCP-1及单个核细胞CCR2表达显著下降（P〈0.05）,PPARβm RNA及蛋白表达均较前增加（P〈0.05）。结论：瑞舒伐他汀可能通过PPARβ途径降低MCP-1,抑制单个核细胞CCR2的表达。

英文摘要：

Objective： To investigate the effect of rosuvastatin therapy on C-C chemokine receptor（CCR2）expression in mononuclear cells in patients with carotid atherosclerosis and explore the possible upstream mechanism. Methods： Twenty patients without previous statin treatment were enrolled. Rosuvastatin were given 5 to 20 mg / day for 3 months. At baseline and 12 weeks,lipid profile and plasma monocyte chemotactic protein-1（MCP-1） levels were examined. The m RNA and protein expressions of CCR2 in the mononuclear cells were measured with RT-PCR and flow cytometry,respectively. The m RNA and protein expression of peroxidase proliferator-activated receptor（PPAR β） were detected with RTPCR and Western blot,respectively. Results： After 3-months rosuvastatin treatment,the patients＇ low-density lipoprotein cholesterol（LDL-C）levels decreased significantly（P 0. 01）. Compared with baseline,the m RNA and protein expressions of CCR2 in the mononuclear cells showed significantly decrease,as well as plasma MCP-1 levels（P 0. 05）. Both m RNA and protein expressions of PPAR β in the mononuclear cells increased（P 0. 05）. Conclusion： Rosuvastatin may attenuate MCP-1 / CCR2 through PPARβ upstream pathway.