Apolipoprotein A1 Mimic Peptide L4F Of Endoplasmic Reticulum Stress Pathway Of Apoptosis In The Regulation Of Vascular Endothelial Cells And Its Mechanism

Objective：The purpose of the present study was to investigate the inhibitory effect of apolipoproteinAI (Apo AI) mimetic peptide L-4F on oxidized low density lipoprotein (ox-LDL)-induced apoptosis ofvascular endothelial cells and the underlying molecular mechanisms，in order to further clarify theantiatherosclerotic mechanism of Apo AI mimetic peptide.Methods：Human umbilical vein endothelial cell EA.hy926were randomly divided into four groups：（1）normal control group：cells were routinely incubated in the culture medium.（2）ox-LDL（100mg/L）group: cells were treated with100mg/L ox-LDL.（3）Scrambled mimic peptide（sL-4F）(100mg/L) group：cells were pretreated with100mg/L sL-4F for1hour and then treated with100mg/Lox-LDL as the negative interventing group.（4）L-4F interventing group： cells were pretreated withdifferent concentrations of L-4F (25,50and100mg/L) for1hour and then treated with100mg/Lox-LDL. After incubation for24hour, the viability and apoptosis of cells was detected by MTT assayand Annexin V-FITC double staining assay, respectively. The integrity of the membrane was evaluatedby lactic dehydrogenase (LDH) release. The protein and mRNA expression of scavenger receptor CD36were detected by western blot and real-time PCR, respectively.Results: Compared with normal control group, the cell viability of ox-LDL group significantlydecreased, while the release of LDH and cell apoptotic rate of early and late phases increasedsignificantly increased. In addition, the expression of CHOP protein and mRNA were significantlyupregulated by ox-LDL. Compared with ox-LDL group, cell viability of L-4F interventing groupincreased significantly, while the release of LDH and cell apoptotic rate of early and late phasesdecreased. Moreover, L-4F significantly inhibited ox-LDL-induced CHOP upregulation at the levelsof protein and transcription.Conclusion:1. L4F, an apo AI mimetic peptide, can reduce ox-LDL-induced apoptosis of vascularendothelial cell;2. The mechanism at least partially involves its ability to inhibit CHOP-mediatedendoplasmic reticulum stress apoptosis pathway.