Xu Zhu-mei, Zhao Shui-ping, Li Quan-zhong, Nie Sai, Zhou Hong-nian
Department of Cardiology, The Second XiangYa Hospital, Central South University, Middle Ren-min Road No. 86, Hunan 410011, Changsha, People's Republic of China.
Clin Chim Acta. 2003 Dec;338(1-2):17-24. doi: 10.1016/s0009-8981(03)00321-8.
The monocyte chemoattractant protein-1 (MCP-1) is a chemokine responsible for the recruitment of monocytes to sites of inflammation. MCP-1 may play critical roles in plaque instability. Anti-inflammation may be one benefit of statin drugs in acute coronary syndrome (ACS). We investigated the effects of atorvastatin therapy on plasma MCP-1 concentrations and production of MCP-1 released by peripheral blood monocytes from ACS patients.
Forty patients with ACS were randomly separated into two groups, those receiving conventional therapy (Group A, n=20), and conventional therapy+atorvastatin (10 mg/day, Group B, n=20). The study the effects of atorvastatin on secretion and expression of MCP-1, human peripheral blood monocytes from healthy donors were incubated with atorvastatin (0.1-10 micromol/l) for up to 24 h in vitro. MCP-1 concentrations in plasma and monocytes culture supernatants were measured by enzyme-linked immunosorbent assays (ELISA). MCP-1 expression was measured by RT-PCR.
Plasma concentrations of MCP-1 were significantly lower after 4 weeks therapy in both groups of patients [Group A from 97.4 (50.1-164) to 72.6 (36.3-156) pg/ml, Group B from 101 (60-178) to 45 (29-91) pg/ml, (P<0.05, respectively)]. Compared with conventional therapy alone, atorvastatin significantly further reduced plasma MCP-1 concentrations. There was no significant correlation between the degree of changes in plasma MCP-1 and LDL-C. In vitro, atorvastatin inhibits production of MCP-1 up to 73%, in a concentration-dependent manner, and suppressed MCP-1 expression in peripheral blood monocytes.
Atorvastatin reduced plasma MCP-1 concentrations in patients with ACS. These effects may explain some clinical benefits of statins in the treatment of these patients.
单核细胞趋化蛋白-1（MCP-1）是一种趋化因子，负责将单核细胞募集到炎症部位。MCP-1可能在斑块不稳定中起关键作用。抗炎作用可能是他汀类药物在急性冠状动脉综合征（ACS）中的益处之一。我们研究了阿托伐他汀治疗对ACS患者血浆MCP-1浓度以及外周血单核细胞释放MCP-1的影响。
40例ACS患者随机分为两组，一组接受常规治疗（A组，n = 20），另一组接受常规治疗加阿托伐他汀（10毫克/天，B组，n = 20）。为研究阿托伐他汀对MCP-1分泌和表达的影响，将健康供体的人外周血单核细胞与阿托伐他汀（0.1 - 10微摩尔/升）在体外孵育长达24小时。采用酶联免疫吸附测定（ELISA）法检测血浆和单核细胞培养上清液中MCP-1的浓度。通过逆转录聚合酶链反应（RT-PCR）检测MCP-1的表达。
两组患者治疗4周后血浆MCP-1浓度均显著降低[A组从97.4（50.1 - 164）降至72.6（36.3 - 156）皮克/毫升，B组从101（60 - 178）降至45（29 - 91）皮克/毫升，（P均<0.05）]。与单纯常规治疗相比，阿托伐他汀能显著进一步降低血浆MCP-1浓度。血浆MCP-1变化程度与低密度脂蛋白胆固醇（LDL-C）之间无显著相关性。在体外，阿托伐他汀以浓度依赖的方式抑制MCP-1的产生达73%，并抑制外周血单核细胞中MCP-1的表达。
阿托伐他汀降低了ACS患者的血浆MCP-1浓度。这些作用可能解释了他汀类药物在治疗这些患者中的一些临床益处。
