[Folate reduces monocyte chemoattractant protein-1 expression in rats with hyperhomocysteinemia].

Zhongguo Yi Xue Ke Xue Yuan Xue Bao

Department of Cardiovasology, Union Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430022, China.

Published: August 2005

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).

Conclusion: 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.

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