| Effects of saturated free fatty acids on the suvival rate of human umbilical vein endothelial cellsABSTRACTObjective To investigate the effects of various free fatty acids, including palmitic acid (PA), stearic acid (SA), oleic acid (OA), linoleic acid (LA) and arachidonic acid (AA), and insulin, leptin and tumor necrosis factor-a (TNF- a ) on the cell survival of human umbilical vein endothelial cell (HUVEC). Methods 1. The cell survival was assessed using MTT method after the cells were treated with various FFAs and other regions. 2. Apoptosis and necrosis of the cells were determined using annexinV-FITC /PI staining by flow cytometry. Results 1. PA and SA markedly suppressed HUVEC survival in a time- and dose-dependent manner. The cell survival was about 45 ?.3 % of the control after treatment with PA and SA at 200 umol/L for 72h. OA killed all of the cells within 48h at 100umol/L There was no effect of LA on the cell survival. While, AA significantly increased the cell number to 128?.1% of the control groups after treatment for 72h at 2 umol/L. 2. The apoptotic Cells rates were 26.8% after HUVEC treated with various PA for 8h. 3. Polyunsaturated FFA AA could partly prevent the cell death induced by PA.Conclusion: Saturated FFA PA and SA, and monounsaturated OA are toxic to HUVEC, while polyunsaturated FFA AA can partly prevent the cytotoxicity induced by PA. PA induced apoptosis at low dose within 4h, but necrosis at high dose and longer time than 4h; These results indicate that not only the concentration of the saturated FFA, but also the ratio of saturated FFA and AA are important for the survival of endothelial cells.The study of the cytotoxic mechanism about saturated fatty acids on vascular endothelial cellsABSTRACTObjective: To explore the mechanism of impaired endothelial cells induced by saturated fatty acids (SFAs) Methods: The substances were chosen, which possibly block the cytotoxic effects of SFAs on varscluar endothelial cell, including calcium channel blockade (Nifedipine), calcium ionophore (A23187), nitric oxide synthase inhibitor (N nitro-L-arginia, L-NNA), inhibitors of ceramide (Fumonisin B1), FKA and PKC inhibitors, PPAFtgamma activator, ProstaglandinE2 (PGE2), vitaminE, The substance (ML-7 ) which could inhibit protein synthetize. The cell survival was assessed using MTT after the cells were treated with PA and thirteen kind substances respectively. Results 1. The cell survival rates significantly increased by 37.5% than that of the group treated by PA alone after treated for 72h by 15umol/L nitric oxide synthase inhibitor (L-NNA) and 200umol/L PA). 2. The cell survival rate significantly decreased by 32.5% comparing with SFAs groups alone. 3.The inhibitors of ceramide had no effect on the cell survival rates (The cell survival rate had no significantly changes comparing with the PA groups alone after treated used for 72h by 5, 10, 15μmol/L CER +200μmol/L PA.) 4.Calcium channel blocker, calcium ionophore, PKA inhibitors, PKC inhibitors, PPARgamma activator, PGE2, Vit E could not yet block the cell death induced by SFAs. Conclusions: 1. Nitric oxide synthase inhibitor (L-NNA ) could block the cell death caused by SFAs. 2.Nitric oxide donors could increased the number of the cell death The results suggested that Excessive nitric oxide production might be the mechanism of the cell death induced by SFAs. 3. The increase of Ca2+ and PGE2 were not associated with the cell death induced by SFAs. The increased activity of PKC and PKA was also unrelated to the cell death induced by SFAs. The reduced activity of PPAR y was not involved in the cell death induced by SFAs.The Role of Nitric Oxide Synthase on Vascular Endothelial Cells Impaired by Saturated Free Fatty AcidsABSTRACTObjectve To demonstrated the mechanism of excessive nitric oxide production during satured fatty acids result in impaired vascular endothelial cells. Methods The reverse transcription polymerase chain reaction (RT-PCR) were used analyzed to assay iNOS and eNOS gene expression of vascular endothelial...
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