RESUMO
<p><b>OBJECTIVE</b>To investigate the regulatory effects of fenofibrate on TNF-alpha-induced CD40 expression and matrix metalloproteinase (MMP) activity in human vascular endothelial cells (HUVECs).</p><p><b>METHODS</b>Quantitative RT-PCR and flow cytometry were employed to evaluate the effect of fenofibrate on TNF-alpha-induced CD40 mRNA and cell surface CD40 expression in HUVECs, and gelatin zymography was used to determine the effect of fenofibrate on the gelatinolytic activities of MMP-2 and MMP-9 in TNF-alpha-stimulated HUVECs.</p><p><b>RESULTS</b>Fenofibrate at the concentrations of 5x10(-5), 1x10(-4) and 2x10(-4) mol/L significantly reduced TNF-alpha-induced increment of CD40 mRNA and cell surface CD40 expressions (P<0.01), with the maximal inhibition achieved at the concentration of 1x10(-4) mol/L. Fenofibrate at 2x10(-4) mol/L did not further decrease CD40 expression induced by TNF-alpha. Fenofibrate significantly inhibited the stimulatory effect of TNF-alpha on MMP-2 and MMP-9 activities in HUVECs.</p><p><b>CONCLUSION</b>Fenofibrate reduces TNF-alpha-induced increment of CD40 expression and MMP-2 and MMP-9 activities in HUVECs.</p>
Assuntos
Humanos , Antígenos CD40 , Genética , Células Cultivadas , Relação Dose-Resposta a Droga , Células Endoteliais , Biologia Celular , Metabolismo , Fenofibrato , Farmacologia , Citometria de Fluxo , Metaloproteinase 2 da Matriz , Metabolismo , Metaloproteinase 9 da Matriz , Metabolismo , Metaloproteinases da Matriz , Metabolismo , RNA Mensageiro , Genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Necrose Tumoral alfa , Farmacologia , Veias Umbilicais , Biologia CelularRESUMO
<p><b>OBJECTIVE</b>To investigate the effects of ligustrazine on nitric oxide (NO), malonaldehyde (MDA) production, release of intracellular lactate dehydrogenase (LDH) and membrane fluidity of the injured human umbilical vein vascular endothelial cell line (ECV-304) with hypoxia and lack of glucose.</p><p><b>METHOD</b>The experiments were performed in culture of ECV-304 injured with hypoxia and lack of glucose in vitro. The released LDH of ECV-304 was measured with automatic biochemistry analyse. NO content of ECV-304 was monitored with colorimetry. Lipid peroxidation of ECV-304 was monitored as MDA with a fluorometric assay. The membrane fluidity of ECV-304 was measured with the fluorescence polarization method.</p><p><b>RESULT</b>After culture ECV-304 in hypoxia and lack of glucose for 24 h, the LDH release, MDA production and the membrane fluidity increased significantly and NO level was decreased. Preincubation of ECV-304 with ligustrazine for 24 h reduced LDH release, MDA production, membrane fluidity increasing and increased the level of NO in ECV-304 due to hypoxia and lack of glucose.</p><p><b>CONCLUSION</b>Ligustrazine has protective effect on injury of ECV-304 induced by hypoxia and lack of glucose.</p>