title: [Folate reduces monocyte chemoattractant protein-1 expression in rats with hyperhomocysteinemia].
abstract: OBJECTIVE
  To investigate effects of supplementation of folate on the expression of monocyte chemoattractant protein-1 (MCP-1) in aortic endothelium and release from peripheral blood mononuclear cells (PBMC) in rats with hyperhomocysteinemia induced by ingestion of excess methionine.
  
  
  METHODS
  Thirty male SD rats were randomly divided into 3 groups (n = 10 for each group): control group (Control), high homocysteinemia group (Hhcy), and folate supplementation group (FA). They were fed with nomal diet, normal diet enriched by 1.7% methionine, and normal diet plus 1.7% methionine and 0.006% folate, respectively, for 45 days. The levels of total plasma homocysteine (Thcy) were measured by high performance liquid chromatography and the concentrations of chemokine MCP-1 released from PBMC stimulated by oxidized low density lipoprotein were detected by enzyme immunoassays. The expression of MCP-1 on aortas of rats was detected by immunohistochemistry and Western blot.
  
  
  RESULTS
  A high methionine diet for 45 days induced hyperhomocysteinemia. Folate supplementation to high-methionine diet significantly decreased plasma Thcy levels (P < 0.01). The expression of MCP-1 in aortic endothelium and the levels of MCP-1 released from PBMC stimulated by oxidized low density lipoprotein were significantly higher in rats of Hhcy group than in rats of control group (P < 0.05, P < 0.01). During supplementation of folate, normalization of Thcy levels was accompanied by a marked reduction of MCP-1 expression in aortic endothelium and by a significant decrease of MCP-1 released from PBMC stimulated by oxidized low density lipoprotein (P < 0.05, P < 0.01).
  
  
  CONCLUSIONS
  Folate supplementation can prevent an elevation of homocysteine levels in the blood and decrease the expression MCP-1 in aortic endothelium and release of MCP-1 from PBMC in rats with hyperhomocysteinemia.
authors.affiliation: Department of Cardiovasology, Union Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430022, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Chen
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Yan-Wen
authors.initials: YW
authors.lastname: Shu
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology / Q000378:metabolism; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000235:genetics; D004730:Endothelium, Vascular / Q000378:metabolism; D005492:Folic Acid / Q000494:pharmacology*; D006710:Homocysteine / Q000097:blood; D020138:Hyperhomocysteinemia / Q000097:blood / Q000139:chemically induced / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008715:Methionine; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D018932:Chemokine CCL2; D006710:Homocysteine; D005492:Folic Acid; D008715:Methionine