title: Atorvastatin reduces plasma MCP-1 in patients with acute coronary syndrome.
abstract: 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.
authors.affiliation: Department of Cardiology, The Second XiangYa Hospital, Central South University, Middle Ren-min Road No. 86, Hunan 410011, Changsha, People's Republic of China.
authors.forename: Zhu-mei
authors.initials: ZM
authors.lastname: Xu
authors.forename: Shui-ping
authors.initials: SP
authors.lastname: Zhao
authors.forename: Quan-zhong
authors.initials: QZ
authors.lastname: Li
authors.forename: Sai
authors.initials: S
authors.lastname: Nie
authors.forename: Hong-nian
authors.initials: HN
authors.lastname: Zhou
mesh_terms: D000069059:Atorvastatin; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D017077:Culture Media, Conditioned / Q000737:chemistry; D005260:Female; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: D018932:Chemokine CCL2; D017077:Culture Media, Conditioned; D006538:Heptanoic Acids; D008055:Lipids; D011758:Pyrroles; D012333:RNA, Messenger; D000069059:Atorvastatin