[Folic acid attenuates homocysteine induced human monocytes chemokine secretion via reducing NADPH oxidase activity].
OBJECTIVE
To investigate the effect of folic acid on homocysteine (Hcy)-induced chemokine secretion and NADPH oxidase activity in human monocytes.


METHODS
Human monocytes from healthy volunteers were incubated with Hcy (100 micromol/L) with or without folic acid (5 micromol/L) for 24 h; MCP-1 and IL-8 were assessed by ELISA. DCFH-DA was added to monitor intracellular ROS production on confocal microscopy. A cytochrome c reduction assay was used to measure NADPH oxidase activity.


RESULTS
The Hcy-induced secretion of MCP-1 and IL-8 was significantly reduced by folic acid [(1.88 +/- 0.51) ng/ml vs. (4.36 +/- 0.72) ng/ml vs. (2.40 +/- 0.60) ng/ml and (4.9 +/- 1.9) ng/ml vs. (12.7 +/- 1.5) ng/ml vs. (7.2 +/- 1.9) ng/ml, all P < 0.05]. The Hcy-induced production of ROS was also significantly attenuated by folic acid. Moreover, the Hcy-induced NADPH oxidase activity increase was significantly inhibited by cotreatment with folic acid.


CONCLUSIONS
Folic acid may attenuate oxidative stress induced by Hcy by reducing NADPH oxidase activity in monocytes.
Wang
Ying
Y
Cardiovascular Medicine, Beijing Haidian Hospital, Beijing 100080, China.
Wang
Guang
G
Zhang
Fu-chun
FC
Mao
Jie-ming
JM
Dai
Jing
J
D002478:Cells, Cultured; D018925:Chemokines / Q000378:metabolism*; D005492:Folic Acid / Q000494:pharmacology*; D006710:Homocysteine / Q000494:pharmacology*; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D019255:NADPH Oxidases / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects; D054390:Receptors, CCR2 / Q000378:metabolism
D018925:Chemokines; D016209:Interleukin-8; D054390:Receptors, CCR2; D006710:Homocysteine; D005492:Folic Acid; D019255:NADPH Oxidases