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Folic acid attenuates homocysteine induced human monocytes chemokine secretion via reducing NADPH oxidase activity / 中华心血管病杂志
Chinese Journal of Cardiology ; (12): 956-959, 2007.
Artículo en Chino | WPRIM | ID: wpr-299549
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of folic acid on homocysteine (Hcy)-induced chemokine secretion and NADPH oxidase activity in human monocytes.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>Folic acid may attenuate oxidative stress induced by Hcy by reducing NADPH oxidase activity in monocytes.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Monocitos / Células Cultivadas / Interleucina-8 / Estrés Oxidativo / Quimiocinas / NADPH Oxidasas / Secreciones Corporales / Receptores CCR2 / Ácido Fólico Límite: Humanos Idioma: Chino Revista: Chinese Journal of Cardiology Año: 2007 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Monocitos / Células Cultivadas / Interleucina-8 / Estrés Oxidativo / Quimiocinas / NADPH Oxidasas / Secreciones Corporales / Receptores CCR2 / Ácido Fólico Límite: Humanos Idioma: Chino Revista: Chinese Journal of Cardiology Año: 2007 Tipo del documento: Artículo