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中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (3): 202-206.doi: 10.13459/j.cnki.cjap.2016.03.003

• 研究论文 • 上一篇    下一篇

瑞舒伐他汀对颈动脉粥样硬化患者单个核细胞CCR2表达的影响及机制

杜瑞雪1, 叶平1, 颜光涛2, 邓子辉2, 梁文涛3, 郭子宽5, 张红红4, 耿淼4   

  1. 1. 解放军总医院南楼心内科, 北京 100853;
    2. 解放军总医院基础医学研究所, 北京 100853;
    3. 解放军总医院普通外科研究所, 北京 100853;
    4. 解放军总医院老年医学研究所, 北京 100853;
    5. 军事医学科学院放射与免疫研究所, 北京 100850
  • 收稿日期:2016-01-22 修回日期:2016-03-07 出版日期:2016-05-28 发布日期:2018-06-12
  • 通讯作者: 叶平,Tel:010-66876369;E-mail:yeping301@sina.com E-mail:yeping301@sina.com
  • 基金资助:
    国家自然科学基金项目(81270941)

The effect of rosuvastatin therapy on CCR2 expression in mononuclear cells and its upstream pathway

DU Rui-xue1, YE Ping1, YAN Guang-tao2, DENG Zi-hui2, LIANG Wen-tao3, GUO Zi-kuan5, ZHANG Hong-hong4, GEN Miao4   

  1. 1. Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853;
    2. Institue of Basic Medical Sciences, Chinese PLA General Hospital, Beijing 100853;
    3. Institute of Surgery, Chinese PLA General Hospital, Beijing 100853;
    4. Institute of Geriatrics, Chinese PLA General Hospital, Beijing 100853;
    5. Radiology and Immunology Institute, Academy of Military Medical Sciences, Beijing 100850, China
  • Received:2016-01-22 Revised:2016-03-07 Online:2016-05-28 Published:2018-06-12
  • Supported by:
    国家自然科学基金项目(81270941)

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)β mRNA的表达;Western印迹法检测PPAR β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),PPAR β mRNA及蛋白表达均较前增加(P<0.05)。结论:瑞舒伐他汀可能通过PPAR β途径降低MCP-1,抑制单个核细胞CCR2的表达。

关键词: 瑞舒伐他汀, 动脉粥样硬化, CC类趋化因子受体2, 过氧化物酶体增生物激活受体β

Abstract: 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 mRNA and protein expressions of CCR2 in the mononuclear cells were measured with RT-PCR and flow cytometry, respectively. The mRNA and protein expression of peroxidase proliferator-activated receptor(PPAR β) were detected with RT-PCR 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 mRNA and protein expressions of CCR2 in the mononuclear cells showed significantly decrease, as well as plasma MCP-1 levels (P<0.05). Both mRNA 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.

Key words: rosuvastatin, atherosclerosis, CCR2, PPAR β

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