title: Folic acid reduces chemokine MCP-1 release and expression in rats with hyperhomocystinemia.
abstract: OBJECTIVE
  This study aimed to investigate the effects of folate on the monocyte chemoattractant protein-1 (MCP-1) expression and release in rats with hyperhomocystinemia induced by ingestion of excess methionine.
  
  
  RESULTS
  Thirty male Sprague-Dawley rats (200+/-20 g) were randomly divided into three groups (n=10 for each group): control group (Control), high-homocystinemia (Hhcy) group, and folate treatment (FA) group. They were fed with a normal regular diet, enriched by 1.7% methionine plus 1.7% methionine and 0.006% folate for 45 days. Our study showed the following: (a) A high methionine diet for 45 days is sufficient to induce hyperhomocystinemia; folate supplementation to the rats fed the high-methionine diet prevented an elevation homocysteine (Hcy) levels in the blood (P<.01). (b) Compared with the Control group, the Hhcy group had elevated plasma levels of MCP-1, and Hcy was significantly correlated with MCP-1 (P<.05). (c) The protein and mRNA expression of MCP-1 in the aorta was higher in rats from the Hhcy group than in rats from the Control group. (d) Most important, after folic acid supplementation, the lowering of Hcy levels was accompanied by a marked reduction of MCP-1 expressed in aortae and released from plasma and peripheral blood mononuclear cells (PBMCs) stimulated by oxidized low-density lipoprotein (P<.05, P<.01).
  
  
  CONCLUSIONS
  Folic acid supplementation not only can blunt the rise in Hcy and reduce MCP-1 released from both plasma and PBMCs of rats with hyperhomocystinemia but also can downgrade MCP-1 expression in the aorta of rats with hyperhomocystinemia.
authors.affiliation: Institute of Cardiovasology, Union Hospital, Tongii Medical College, Huazhong Science and Technology University, Hubei, China. liming518888cn@yahoo.com.cn
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Jian
authors.initials: J
authors.lastname: Chen
authors.forename: Yu-Shu
authors.initials: YS
authors.lastname: Li
authors.forename: Yi-Bai
authors.initials: YB
authors.lastname: Feng
authors.forename: Qiu-Tang
authors.initials: QT
authors.lastname: Zeng
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism; D015153:Blotting, Western; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D005492:Folic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D006710:Homocysteine / Q000097:blood; D020138:Hyperhomocysteinemia / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D007150:Immunohistochemistry; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008715:Methionine; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014803:Vitamin B Complex / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D008077:Lipoproteins, LDL; D012333:RNA, Messenger; C099252:oxidized low density lipoprotein; D006710:Homocysteine; D014803:Vitamin B Complex; D005492:Folic Acid; D008715:Methionine