The Mechanism Of Vaccinic And Elaidic Acids Induced Inflammation Of Human Umbilical Vein Endothelial Cells

Dietary trans fatty acids(TFAs)had attracted public concern for a long time,which were reported to induce chronic disease,especially coronary heart disease(CHD).TFA mainly came from industrial hydrogenated oil and ruminant products,and the predominant isomers of industrial TFA(I-TFA)and ruminant TFA(R-TFA)were elaidic acid(9t18:1,EA)and vaccenic acid(11t18:1,VA),respectively.I-TFA had been demonstrated to be positive with CHD from many epidemiology studies,hence,a reduction of TFA consumption was promoted in many countries.While TFA also originated from ruminant products,whether the R-TFA had the same effects on CHD as I-TFA and whether the ruminant products should be limited were still in discussion.The studies of clinic and animal reported that EA could increase NF-?B activation and impair insulin-mediated NO production in endothelial cells while VA was not associated with these responses.Using the endothelial cell,Wen find out the effect of EA and VA on endothelial cell with the same dosage of purified VA and EA,and exclude other dietary component intervention.Precious study from our lab observed that endothelial cells injury induced by VA was significantly weaker than that of EA.From those studies,it seemed that EA was related to the endothelial cell dysfunction,while VA had shown no association or weak association with endothelial cell dysfunction.In humans,the conversion of VA to 9c11t-CLA via stearoyl-CoA desaturase(SCD)had ranged from 11 to 30%.9c11t-CLA had been demonstrated to reduce CHD risk in animal and clinical studies.It is not clear,whether and to what extent the difference between VA and EA was contribute to the VA bio-conversion or the VA self-mediated.Based on the results of which Wen study.Thus,our study objective to the expression of which adhesive factor,pro-inflammatory factor,TLR4 protein and MAPKs protein(ERK1/2,p38 MAPK,JNK1/2)in HUVECs,effect of different source trans fatty acid stimulated the cell viability and inflammatory response by SCD inhibitor(leptin)and 9c11t-CLA,to studies TLR4 protein expression and play a role in TFAs stimulated inflammation.To explain the reason of which different injure mechanism of HUVECs co-cultivated with VA and EA,which could provide a scientific basis for prevention and treatment of cardiovascular disease cause by FA.The mian results obtained are as follows,1.11t18:1 partially transformed to 9c11t-CLA.The conversion of VA transfer to 9c11t-CLA was 23.1±0.79% via stearoyl-CoA desaturase(SCD)in HUVECs.2.9c11t-CLA has a regulatory effect on inflammation of HUVECs.The objective of this study was to explore the reason of difference between elaidic acid(9t18:1)and vaccenic acid(11t18:1)in endothelial cells dysfunction.Our results illustrated that compared to cells treated with 11t18:1 and 11t18:1+leptin,cell viability increased,NOS-NO system vitality increased,the mRNA expression levels of inflammatory factors(ICAM-1,VCAM-1,IL-6)secretion decreased and the levels of MAPKs activation decreased in cells treated with supplemented 9c11t-CLA groups,respectively.9c11t-CLA was improtant factor which 11t18:1 different with 9t18:1 induced inflammation of HUVECs.3.11t18:1 induced inflammation of HUVECs.Compared to cells treated with 11t18:1,cell viability decreased,NOS-NO system vitality decreased,the mRNA expression levels of inflammatory factors(ICAM-1,VCAM-1,IL-6)secretion increased and the levels of MAPKs activation increased in cells treated with 11t18:1+leptin,and elucidate VA-self does not has anti-inflammatory effect in HUVECs.The difference between VA and EA was contribute to the VA endogenous but the VA self-mediated,and the mechanism of MUFAs-mediated immunomodulatory activities was provided.4.TLR4 pathway involve in TFAs stimulated inflammation of HUVECs TLR4 pathway involve in mono-unsaturated fatty acids(MUFAs)stimulated inflammatory cytokines secretion of HUVECs.Our previous study showed that trans fatty acids(TFAs)can cause inflammation of endothelial cells through the TLR4-meditated MAPKs pathway and stimulated inflammatory cytokines in HUVECs.