Inhibitory effect of querctin on metalloproteinases expression and LPS-induced nitric oxide production.

SARAGUSTI ALEJANDRA; ORTEGA GABRIELA; CABRERA JOSE LUIS; CHIABRANDO GUSTAVO

Pinamar

Congreso; XLI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB) 2005. X Congreso de la Panamerican Association for Biochemistry and Molecular Biology (PABMB) 2005. XX Reunión Anual de la Sociedad Argentina de Neuroquí; 2005

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB)

INHIBITORY EFFECT OF QUERCETIN ON METALLOPROTEINASES EXPRESSION AND LPS-INDUCED NITRIC OXIDE PRODUCTION Saragusti A, Ortega G, Cabrera JL and Chiabrando GA CIBICI and IMBIV (CONICET). Facultad de Ciencias Químicas. Universidad Nacional de Córdoba. Quercetin (QT) is a flavonoid with anti-inflammatory activity, although the molecular mechanisms are unclear yet. During inflammation Metalloproteinases (MMPs) and Nitric Oxide (NO) play a key role; however in severe inflammatory stages (acute and chronic) have deleterious consequences. In this work, the main objective was to investigate the anti-inflammatory effect of Qt, evaluating the inhibitory action on MMPs (MMP-2 and MMP-9) and NO production. The inhibitory Qt effect on MMPs activity was analyzed by zymography in conditional culture medium of CHOK-1 cell incubated in the presence of QT (from 25 to 100 uM). In addition, levels of MMP-2 and MMP-9 mRNAs were determined by RT-PCR. Finally, the LPS-induced NO production was measured by Griess reaction in the conditional culture medium of J774 macrophages cell line incubated in the presence of Qt (from 25 to 100 uM). The results showed that Qt inhibited the MMPs expression at the activity and transcriptional levels. Inhibitory effects were also observed in the LPS-induced NO production. These results taken together indicate that Qt exerts its anti-inflammatory effect by inhibiting the main components of inflammation stages, such as MMPs and NO, which could suggest that this flavonoid affects the signalling pathways involved in the regulation of these inflammatory mediators.