PMID- 14637261 OWN - NLM STAT- MEDLINE DCOM- 20040714 LR - 20220311 IS - 0009-8981 (Print) IS - 0009-8981 (Linking) VI - 338 IP - 1-2 DP - 2003 Dec TI - Atorvastatin reduces plasma MCP-1 in patients with acute coronary syndrome. PG - 17-24 AB - BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. FAU - Xu, Zhu-mei AU - Xu ZM AD - Department of Cardiology, The Second XiangYa Hospital, Central South University, Middle Ren-min Road No. 86, Hunan 410011, Changsha, People's Republic of China. FAU - Zhao, Shui-ping AU - Zhao SP FAU - Li, Quan-zhong AU - Li QZ FAU - Nie, Sai AU - Nie S FAU - Zhou, Hong-nian AU - Zhou HN LA - eng PT - Clinical Trial PT - Journal Article PT - Randomized Controlled Trial PL - Netherlands TA - Clin Chim Acta JT - Clinica chimica acta; international journal of clinical chemistry JID - 1302422 RN - 0 (Chemokine CCL2) RN - 0 (Culture Media, Conditioned) RN - 0 (Heptanoic Acids) RN - 0 (Lipids) RN - 0 (Pyrroles) RN - 0 (RNA, Messenger) RN - A0JWA85V8F (Atorvastatin) SB - IM MH - Atorvastatin MH - Cells, Cultured MH - Chemokine CCL2/analysis/*blood/genetics/metabolism MH - Coronary Disease/*blood/drug therapy/genetics/metabolism MH - Culture Media, Conditioned/chemistry MH - Female MH - Heptanoic Acids/*pharmacology/therapeutic use MH - Humans MH - Lipids/blood MH - Male MH - Middle Aged MH - Monocytes/drug effects/metabolism MH - Pyrroles/*pharmacology/therapeutic use MH - RNA, Messenger/genetics/metabolism EDAT- 2003/11/26 05:00 MHDA- 2004/07/15 05:00 CRDT- 2003/11/26 05:00 PHST- 2003/11/26 05:00 [pubmed] PHST- 2004/07/15 05:00 [medline] PHST- 2003/11/26 05:00 [entrez] AID - S0009898103003218 [pii] AID - 10.1016/s0009-8981(03)00321-8 [doi] PST - ppublish SO - Clin Chim Acta. 2003 Dec;338(1-2):17-24. doi: 10.1016/s0009-8981(03)00321-8.