EFFECTS OF QUERCETIN ON MEMBRANE FLUIDITY OF INJURED VASCULAR ENDOTHELIAL CELLS WITH HYPOXIA AND THE LACK OF GLUCOSE

Vascularendothelialcellsinhypoxiaandthelackofglucosecanproducealotofactiveoxygen ,whichresultsinthedamageofendothelialcells .Furthermore,dysfunctionofvascularendothelialcellsistheinitiativestepofatherosclerosisandmayleadtosomeofcardiovasculardiseases[1 ,2 ] .So ,theprotectionofendothelialcellsfromtheinjuryplaysanimportantroleinthepreventionandtreatmentofatherosclerosis,hypertension ,hyperc holesterolaemiaandsoon .Therefore,manyre searchershavebeenlookingforamedicinethatcanhelptomaintainthenorm…

EFFECTS OF QUERCETIN ON MEMBRANE FLUIDITY OF INJURED VASCULAR ENDOTHELIAL CELLS WITH HYPOXIA AND THE LACK OF GLUCOSE

Objective To study the effects of different concentrations of Quercetin on nitric oxide (NO) production and membrane fluidity of the injured human umbilical vein vascular endothelial cell line(ECV-304) with hypoxia and the lack of glucose. Methods The experiments were performed in the culture of ECV-304 injured with hypoxia and the lack of glucose in vitro. The releases of intracellular lactate dehydrogenase(LDH) of ECV-304 was measured with automatic biochemistry analysis. NO level of ECV-304 was monitored with colorimetry. The membrane fluidity of ECV-304 was measured with the fluorescence polarization method. Results After ECV-304 was cultured in hypoxia and the the lack of glucose for 24 hours, the release of LDH and the membrane fluidity were increased significantly; NO level was decreased. Preincubation of ECV-304 with 20, 80,160μmol*L-1 of Quercetin for 24 hours reduced LDH activity, membrane fluidity and increased the level of NO in hypoxia and the lack of glucose induced ECV-304. Conclusion These results demonstrate that Quercetin can produce the protective effect on hypoxia and the lack of glucose induced injury of ECV-304 by increasing release of NO and changing membrane fluidity.