Abstract:Aim As atherosclerosis developed,it will rupture or plug the vascular lumen when reached a certain extent,thus can affect the blood flow.Atherosclerotic plaque can always be found in carotid artery in which blood flow will supply our brain.Flow reduction will result in a stroke.Carotid endarterectomy(CEA) is one surgical method which will remove the plaque in the carotid artery through surgical method.So that can restore blood flow and prevent stroke.This article describes the development of CEA,evidence-based way,risks and complications,so that will help more clinicians to have a better understand the CEA as well as the relationship between i

Abstract:Aim The present study was undertaken to investigate the possible mechanism of Tongxinluo on preventing vasoconstriction and vascular hypersensitivity to 5-hydroxytryptamine induced by the injury of the adventitia. Methods Wistar Kyoto rats were assigned to 4 treatments(n=12 for each group): vehicle,low dose of Tongxinluo [200 mg/(kg·d)],middle dose of Tongxinluo [400 mg/(kg·d)] and high dose of Tongxinluo [800 mg/(kg·d)].After 1 week of treatment,adventitia injury was induced by positioning a silicone collar around the right carotid artery for one week.Blood flow and vascular reactivity to serotonin were determined 1 week after injury,the blood from the rat's heart was taken to measure the concentration of angiotensinⅡ(Ang Ⅱ) in the serum with the ELISA,and both side of carotids were harvested for RT-PCR analysis. Results Collar-induced adventitia injury decreased the carotid blood flow(P>=0.0002),increased the vascular reactivity sensitivity to 5-hydroxytryptamine,and upregulated the expression of AngⅡ type 1(AT1)receptor(135% increase,P>=0.0020),Ang ⅡII type 2(AT2)receptor(76% increase,P>=0.0061),and p22phox(2.89 fold increase,P><0.0001)in collared arteries.Low dose of Tongxinluo did not affect vasoconstriction function,serum AngⅡconcentration,or the expressions of AngⅡ receptors and p22phox.Treatment with medium dosage and high dosage of Tongxinluo can effectively improve the carotid blood flow,normalize the hypersensitivity to 5-hydroxytryptamine(all with P><0.05),lower serum AngⅡ concentration(middle dosage group:26.31±6.82 ng/L vs 45.21±4.52 ng/L,P>=0.0480;high dosage group: 20.51±2.51 ng/L vs 45.21±4.52 ng/L,P>=0.0183),restrained the increase of p22phox expressions(79.1% decreasing in middle dosage group,P>=0.0002;83.2% decreasing in high dosage group,P>=0.0001),did not affect the AT1 receptor expression,while high dose of Tongxinluo increased AT2 receptor expression. Conclusion Tongxinluo can effectively prevent the vasoconstriction and the vascular hypersensitivity to 5-HT induced by the adventitia injury in rat carotid through lowering serum AngⅡ level and restraining the significantly enhanced oxidative stress induced by the adventitia injury.

Abstract:Aim To investigate the effects of rosiglitazone on the proliferation of vascular smooth muscle cells induced by angiotensinⅡ(AngⅡ) and possible mechanism. Methods Vascular smooth muscle cells(VSMC) were isolated from aortic media of four-week-old male Sprague-Dawley rats by enzymatic digestion and cultured in monolayer.VSMC in passage 4～8 in log phase were used in following experiments.VSMC were treated by 1 μmol/L AngⅡ for 6 h and randomly divided into the groups as follows: control group(10% FBS in DMEM),Ang Ⅱ group(1 μmol/L AngⅡ),groups respectively treated with different concentration of rosiglitazone(20,30,40 and 50 μmol/L) for 12 h and groups respectively treated with 30 μmol/L rosiglitazone for 6,12,18 and 24 h.The VSMC growth,change of proliferation cycle and mRNA and protein expression of AngⅡ type 2 receptor(AT2R) in all groups were detected by using MTT colorimetric assay,FCM,RT-PCR and Western blotting. Results The mean absorbance(A value) in the VSMC treated by AngⅡ was significantly higher as compared with that of the control group(P><0.01).The A values were markedly reduced in the VSMC treated by different concentration of rosiglitazone for 12 h or 30 μmol/L rosiglitazone for 6,12,18 and 24 h(P><0.05 or P><0.01).The proliferation index(PI) and S-phase fraction(SPF) in the AngⅡ group were significantly higher than those of the control group(P><0.01).With the increase in rosiglitazone concentration and prolongation of treatment time,PI and SPF were greatly reduced(P><0.05 or P><0.01).Compared with the AngⅡ group,expression of AT2R mRNA and protein in the VSMC with the treatment of 20,30 and 50 μmol/L rosiglitazone for 12 h or of 30 μmol/L rosiglitazone for 6,12 and 24 h were both markedly increased(P><0.05 or P><0.01),reaching a maximum in 50 μmol/L rosiglitazone for 12 h or 30 μmol/L rosiglitazone for 24 h. Conclusions Rosiglitazone inhibited VSMC proliferation induced by AngⅡ at least partially through up-regulating expression of AT2R both at mRNA and protein levels in a concentration-dependent and time-dependent manner,in order to play vasculoprotective role.

Abstract:Aim To establish the model of murine macrophage RAW264.7 derived foam cell and identify them with simple and accurate method. Methods The experiment was devided into normal control group and six experimental groups of different concentration of oxidized low density lipoprotein(ox-LDL) incubated with cell.On the incubation time for 24 hours that MTT method and flow cytometry(FCM) were used to determine the suitable range of ox-LDL concentration,then measure intra-cellular cholesterol ester in different level of macrophage foam cell with total cholesterol and free cholesterol kit. Results Cell viability had been significantly inhibited when ox-LDL concentration was at the range of 20～30 mg/L,when ox-LDL concentration was greater than 40 mg/L,apoptosis cells continuously necrosis.Ox-LDL at the concentration of 20 and 30 mg/L,incubated with cell for 24 hours,the propotion of intra-cellular cholesterol ester were 66.26% and 71.19%.Foam cell induced by 10 mg/L of ox-LDL was not typical,and by 40 mg/L of ox-LDL or more,severe degree of foam cell led to cells floating,most cells were rupture or apoptosis,lipid droplet dispersed in extra-cellular. Conclusion Ox-LDL at the concentration range of 20～30 mg/L,incubated with RAW264.7 for 24 h,induced foam cell has good morphology,and model stability,meet the morphology feature of foam cell.

Abstract:Aim To investigate whether ischemia-induced neovascularization is impaired in diabetic mice and the effect of insulin administration on this dysfunction and the underling mechanisms. Methods Unilateral hindlimb ischemia was performed in streptozotocin-induced diabetic mice(C57BL/6) by left femoral artery ligation.The plasma vascular endothelial growth factor(VEGF) and stromal-derived growth factor 1α(SDF-1α) levels were measured by ELISA before ligation and 1,3,7,14 days after ischemia.Capillary density was determined in both ischemic and non-ischemic gastrocnemius muscles by CD31 staining.The local expressions of VEGF,endothelial nitric oxide synthase(eNOS),phospho-eNOS,protein kinase B(PKB,Akt) and phospho-Akt were quantified by Western blotting. Results After ischemia,diabetic mice showed abrogated capillary density increase in the ischemic tissue compared with non-diabetic mice(day7: 7.65±1.74 vs 18.22±3.77,P><0.05),which were accompanied by impeded release of plasma VEGF and SDF-1α(P><0.01),and impaired upregulation of local VEGF protein expression as well as Akt and eNOS phosphorylation(P><0.05).Insulin administration significantly ameliorated ischemia-induced angiogenesis in treated compared with non-treated diabetic groups(15.36 ± 2.14 vs 7.65 ±1.74,P><0.05),elevated plasma levels of VEGF and SDF-1α(P><0.01),as well as enhanced local VEGF expression and Akt/eNOS phosphorylation(P><0.05). Conclusion The data suggested that insulin administration efficiently improved impaired ischemia-induced neovascularization in diabetic mice which may be attributed to restoration of attenuated SDF-1α/VEGF/Akt/eNOS activation.

Abstract:Aim To investigate the effects of fetal intrauterine chromic hypoxia on the vascular endothelial function of adult offspring rats,and its relation to gender,hyperlipemia,and adult hypoxia. Methods Four factorial experiment was designed to explore the role of fetal intrauterine chromic hypoxia,gender,hyperlipemia,and adult hypoxia on endothelial dependent diastolic function.Four animal models of intrauterine chromic hypoxia,hyperlipemia and adult hypoxia were established in Sprague-Dawley rats.Endothelial dependent diastolic function and histologic changes were determined in the rats offsping. Results Except the factor of gender,the other three factors of intrauterine hypoxia,hyperlipemia,and adult hypoxia resulted in an impairment of endothelial dependent diastolic function with main effects of 14.1%,14.2%,12.9%,respectively(all P><0.01).There was a positive interaction between intrauterine hypoxia and hyperlipemia on endothelial function(F=4.889,P><0.05),but no other significant interactions among these four factors.Furthermore,marked histological changes,such as edema,necrosis,and desquamation of vascular epithelium,platelet aggregation and microthrombosis,subendothelial edema and infiltration of inflammatory cells,were observed in the fetal hypoxia offspring but not in the control group. Conclusion Intrauterine chromic hypoxia can induce both functional and morphologic impairment in vascular endothelium from adult offspring rats.This effect on the impaired endothelial function was similar to hyperlipemia and adult hypoxia on that,and was enhanced with hyperlipemia.

Abstract:Aim To explore the infectivity of human cytomegalovirus(HCMV) in vascular smooth muscle cells and provide a cellular model to the mechanism research of atherosclerosis and transplant vasculopathy induced by this virus. Methods Vascular smooth muscle cells were isolated from umbilical arteries,and HCMV with 1 MOI was co-cultured with these cell,the proliferation of virus in these cells was assured by cytopathic effect,the expression of HCMV IE gene,and virus particles observed by electric microscope. Results Cytopathic effect was observed three days post-infection,and HCMV immediate early(IE) gene was expressed in these cells post-infection by RT-PCR,the correctness was assured by DNA sequencing.With electronic microscope technique,the virus particles were observed in these cells. Conclusion HCMV can infect vascular smooth muscle cells and establish proliferating infection.The work provide a model for the research of mechanisms of atherosclerosis and transplant vasculopathy induced by human cytomegalovrirus.

Abstract:Aim To study the expression of CD34 in human coronary atherosclerotic lesions,and the correlation between the expression of CD34 and the lesion types of coronary atherosclerosis,the degree of luminal stenosis and its significance. Methods 312 of coronary artery tissue samples were selected in 53 cases of autopsy.Coronary atherosclerotic lesion and its types were diagnosed by light microscope,and CD34-positive microvessels and CD68-positive macrophages in coronary atherosclerotic lesion were counted by immunohistochemistry. Results CD34-positive microvessels in intima of coronary atherosclerotic lesions were increased with progress of coronary atherosclerotic lesions and aggravation of luminal stenosis with positive correlation(r=0.344,r=0.284,P><0.01),respectively,and the number of CD34-positive microvessels had significant differences between early lesions(typeⅠ-Ⅲ) and advanced lesions(Ⅳ-Ⅵ,P><0.05);The number of CD34-positive microvessels had significant difference between normal cholesterol and hypercholesterolemia(P><0.05);CD68-positive macrophages in intima of coronary atherosclerotic lesions mainly distributed around the CD34-positive blood microvessels,and had positive correlation with CD34-positive microvessels(r=0.303,P><0.01). Conclusion CD34-positive neo-microvessels in intima of human coronary atherosclerosis are increased along with the progress of coronary atherosclerotic lesions and the aggravation of luminal stenosis and the increased infiltration of CD68-positive macrophages and hypercholesterolemia facilitate angiogenesis in atheromatous plaque of coronary atherosclerosis.

Abstract:Aim To investigate the expression of angiotentionⅡ type 2 receptor(AT2) and the effect of rosuvastatin on it after vascular balloon injury in rats. Methods Rat models of aortic endothelial denudation were established by 2F balloon catheters.Rats were randomly allocated into three groups: control group,vascular balloon injury group and rosuvastatin treatment group.The expression of AT2 mRNA and protein were investigated at day 14 and 28 after injury by reverse transcription-polymerse chain reaction(RT-PCR) technique and immunohistochemistry method,respectively. Results Significant intimal thickening was observed at 14 days and 28 days after injury.Rosuvastatin significantly prevented intimal thickening at 14 days and 28 days after balloon injury.The expression of AT2 mRNA and protein increased significantly at 14 days and 28 days after injury(P><0.05),and they increased obviously after rosuvastatin treatment(P><0.05). Conclusion The expression of AT2 mRNA and protein increased significantly after endothelial injury,and rosuvastatin upregulated the expression of AT2.

Abstract:Aim To investigate the effects of streptococcus mutans on the expression of toll-like receptor 2(TLR2),TLR4,interleukin-6(IL-6) and IL-8 in EAhy926 cells(the human endothelial hybridoma of human umbilical vein endothelial cells(HUVEC) and the human epithelial cell line A549,characterized by endothelial phenotype and biology). Methods EAhy926 cells were treated with Streptococcus mutans.The mRNA expression of TLR2,TLR4,IL-6 and IL-8 in EAhy926 cells was detected by reverse transcription polymerase chain reaction(RT-PCR).TLR2 and TLR4 were analyzed by flow cytometry.The production of IL-6 and IL-8 in the cultured supernatants was measured by biochemical method and ELISA respectively.TLR2 and TLR4 blocking assay was used to investigate the relationship between IL-6,IL-8 and TLR2,TLR4 mRNA expression. Results The expression of mRNA and protein for TLR2 and TLR4 in EAhy926 cells increased after stimulated by Streptococcus mutans,peaked the maximal level at 6 h(P><0.05),and then decreased.The expression of IL-6 and IL-8 mRNA was significantly induced when exposed to Streptococcus mutans,reaching the maximal level at 12 h,respectively(P><0.05).Meanwhile,Streptococcus mutans induced the production of IL-6 and IL-8 with peaking at 12 h(P><0.01).The mRNA expression of IL-6 and IL-8 in EAhy926 cells was significantly blocked by anti-human TLR2 and anti-TLR4. Conclusion Streptococcus mutans upregulated the expression of TLR2 and TLR4 and induced the production of inflammatory cytokines IL-6 and IL-8.The expression of TLR2 and TLR4 of EAhy926 cells may elicit a TLR2 and TLR4-mediated innate immune response and contribute to production of inflammatory cytokines IL-6 and IL-8.

Abstract:Aim To investigate the relationship between the single nucleotide polymorphism(SNP) of TNFRSF1B gene and coronary heart disease(CHD) in Chinese population. Methods The polymerase chain reaction-ligase detection reaction(PCR-LDR) was used to detect TNFRSF1B gene rs1061624 in the 104 controls and 208 coronary heart disease patients. Results The frequency of this polymorphism was consistent with the law of Hardy-Weinberg.The frequency of rs1061624 genotype did not differ between the patients and the controls(13.7% vs 18.2%,P>0.05).These results was independent on age,gender,hypertension,diabetes and hyperlipidemia. Conclusion The results support that there is no significant correlation between the polymorphism of TNFRSF1B rs1061624 and coronary heart disease.

Abstract:Aim and Methods The change of cerebrovascular hemodynamic index(CVDI)and Doppler expression of 26 patients with cerebrovascular atherogenesis using the surveying instrument of cerebrovascular hemodynamics were studied. Results ①In most of the patients two sides of total cerebral blood flow and the velocity didn't decrease,the cerebrovascular resistance,elasticity and cvitical pressure increased.The function of cerebrovascular regulation deteriorated.②The Trans-Link Doppler found: the blood flow and the velocity of anterior cerebrovascular artery,middle cerebrovascular artery were in normal range.Cerebral vascualr atherogenesis index especially the(Pulstility P1) increased.③The CVDI had remarkable changes in the lesion side of brain hemisphere,especially the total cerebral blood flow and the velocity decreased. Conclusion The cerebrovascular resistance and the function of cerebrovascular regulation are more serious than that of cerebrovascular atherogenesis.

Abstract:Aim To investigate the predicting value of plasma levels of soluble CD40L(sCD40L),monocyte chemotactic protein-1(MCP-1),interleukin-8(IL-8),and interleukin-6(IL-6) for the severity and instability of coronary artery disease. Methods sCD40L,MCP-1,IL-8 and IL-6 were measured in 129 cases of coronary artery disease patients,including 39 stable angina pectoris,43 unstable angina pectoris and 47 acute myocardial infarction,using flow cytometric method.Gensini scores were evaluated for each patient.Correlation of the above inflammatory factors with Gensini scores was analyzed.The predicting value of the above biomarkers for acute coronary syndrome was investigated. Results Concentrations of the tested inflammatory factors were higher in all the three coronary artery disease groups than those in contrast(all P><0.01).Concentrations of sCD40L,MCP-1 and IL-6 were increased in acute myocardial infarction patients than stable angina pectoris patients(P>=0.001,P>=0.009,P>=0.011,respectively).Plasma concentrations of both MCP-1 and IL-6 manifested positive correlation with Gensini scores(r=0.322,P><0.00001;r=0.203,P>=0.026,respectively).Multiple Logistic regression analysis showed that IL-6 could predict acute coronary syndrome(Or=1.275,P>=0.037). Conclusion The plasma concentrations of sCD40L,MCP-1,IL-8 and IL-6 can predict the existence of atheroma;MCP-1 and IL-6 levels correlate to the severity of atheroma in coronary artery disease patients;IL-6 plays a role in predicting acute coronary syndrome.

Abstract:Aim To investigate the changes in the number and function of endothelial progenitor cells(EPC) from peripheral blood in patients with low extremity arteriosclerosis disease(LEAD). Methods Sixty cases were divided into LEAD group(n=30) and control group(n=30).Mononuclear cells(MNC) were isolated from peripheral blood by density gradient centrifugation.After 7 days induced diferentiation,the adherent cells were identified as EPC by fluorescein staining and flow cytometry.EPCs's number,proliferation,migration and adhesion were assayed by Giemsa's staining,MTT chromatometry,modified Boyden chamber assay and adhesion activity assay. Results The number of EPC was significantly reduced in patients with LEAD compared with control group(27.2±3.6∶52.6±5.9,Cells/×200 fields,P><0.05) and the number of cell clusters was also reduced in patients with LEAD compared with control group(16.6 ±4.8∶22.3±4.9,CFU/×40 fields,P><0.05).In addition,the proliferation(0.193±0.064∶0.243±0.078,P><0.05),migration(12.1±2.7∶17.8±4.2,Cells/×200 fields,P><0.05) and adhesion(47.3±4.3∶51.9±3.7,Cells/×200 fields,P><0.05) in patients with low extremity arteriosclerosis disease were impaired respectively. Conclusion EPC number and function are abnormally decreased in patients with low extremity arteriosclerosis disease.

Abstract:Aim To investigate the relationship between plasma homocysteine(Hcy),polymorphisms of the methylenetetrahydrofolate reductase(MTHFR) gene and atherosclerotic cerebral infarction. Methods Plasma Hcy,polymorphisms of the MTHFR gene in 68 patients with atherosclerotic cerebral infarction(CI) and 50 controls were measured by fluorescence polarization immunoassay(FPIA) and polymerase chain reaction and restriction fragment length polymorphism(PCR-RFLP) respectively. Results The frequencies of TT genotype and T allele were significantly higher in CI group than in controls(P><0.05).Plasma Hcy levels was significantly higher in CI group than in controls(P><0.05).The homocysteine concentration was significantly higher in TT genotype than CT and CC genotypes both in CI group and in control group(P><0.05). Conclusion Elevated Hcy levels is a risk factor for atherosclerotic cerebral infarction.MTHFR C677T polymorphism was significantly related to plasma Hcy levels and atherosclerotic cerebral infarction.

Abstract:Aim To explore the disposition of plasma NT-proBNP level in the community cohort. Methods 734 subjects with high risks of cardiovascular diseases in Beijing Shougang community were investigated.The plasma NT-proBNP level were measured with the automated electrochemiluminescence immunoassay.Their history of myocardial infarction,angina pectoris,hypertension,atrial fibrillation,and diabetes mellitus were collected,their cardiac function were also evaluated with New York Heart Association functional classification.The left ventricular ejection fraction(LVEF) were measured by Echocardiography.To the normal LVEF subjects,they were put in different diastolic heart function groups(the normal one,the mild-damaged and the moderate/severe damaged ones) according to mitral inflow,annulus of mitral valve tissues and pulmonary venous flow of echocardiography.Then the disposition of plasma NT-proBNP level in the community cohort were analyzed. Results The percentage of NYHA functional class Ⅰ and class Ⅱ were 86.5% and 12.9%,and LVEF less than 50% was 3.5%.The median of plasma NT-proBNP level was 69.75 ng/L.The plasma NT-proBNP level in the group with coronary artery disease was higher than that in the group without coronary artery disease(108.60 ng/L vs 65.68 ng/L,P><0.05),the plasma NT-proBNP level in the group with hypertension was higher than that in the group without hypertension(72.71 ng/L vs 61.51 ng/L,P><0.05),the plasma NT-proBNP level in the group with atrial fibrillation was higher than that in the group without atrial fibrillation(93.31 ng/L vs 67.61 ng/L,P><0.05),and the plasma NT-proBNP level in the group with diabetes mellitus was higher than that in the group without diabetes mellitus(80.05 ng/L vs 66.04 ng/L,P><0.05).It was found that the plasma NT-proBNP level in the group of NYHA functional class Ⅱ was higher than that in the group of class Ⅰ(115.5 ng/L vs 65.01 ng/L,P><0.05),and the plasma NT-proBNP level in the lower LVEF group was higher than that in the normal LVEF group(293.8 ng/L vs 67.85 ng/L,P><0.05).In the group with normal LVEF,the plasma NT-proBNP level in the group with different diastolic heart function were 53.73 ng/L,75.07 ng/L,101.85 ng/L and 269.75 ng/L. Conclusion Although the plasma NT-proBNP level in the community cohort is low,but it may be a biochemical marker to monitor the change of their heart function which results in various kinds of cardiovascular diseases.

Abstract:Aim To study the clinical value of interferon-γ,interleukin-10 and CRP in acute coronary syndrome. Methods Using a high sensitivity multiplex assay,previously untested in the context of atherosclerotic disease,we determined plasma concentrations of interferon-γ,interleukin-10,CRP,interleukin-2,interleukin-6,interleukin-8,TNF-α,interleukin-1β,interleukin-12p70 and GM-CSF in 68 acute myocardial infarction(AMI) patients,28 unstable angina(UA) patients and 22 healthy controls. Results Interferon-γ and CRP levels were significantly higher in AMI compared to UA group(P><0.05) and control group(P><0.05).Interleukin-10 also showed higher expression levels in AMI group compared to UA group and control group(P><0.05). Conclusion This up-regulation may reflect the extent of plaque instability and/or rupture in MI patients.Our observations provide evidence that interferon-γ,interleukin-10 and CRP merit further investigation in atherosclerotic disease states as potential markers of disease and therapeutic targets.

Abstract:Aim To investigate the relationship between platelet CD62P and CD63 expression and acute cevebral infarction(ACI). Methods The expression of CD62P,CD63 was detected by flow cytometry in 61 patients with acute cevebral infarction(ACI),and 59 healthy control subjects. Results CD62P,CD63 in acute cevebral infarition were 6.26%±1.68% vs 2.32%±1.14%,6.14%±1.89% vs 2.88%±1.15% respectively,and the result has statistical significance compa with those of the control group(P><0.01). Conclusion The formation of thrombus in actute cerebral infaration patients is highly related to the platelets activation,which can be a diagnostic indicator of cevebral infarction disease.

Abstract:Aim Measurable C-reactive protein using high sensitive method was so called high-sensitivity C-reactive protein.C-reactive protein plays an increasingly important role in the diagnosis and prediction of coronary heart disease and peripheral vascular disease according to a number of researches,more and more studies have revealed C-reactive protein directly involved in cardiovascular diseases,such as inflammation and atherosclerosis.Furthermore,it is one of the most powerful predictors of cardiovascular disease risk factors.All kinds of inflammation,tissue infection and damage will increase the levels of several plasma proteins in circulation,including C-reactive protein as an acute phase reactive protein,and its increased level is a sensitive indicator of inflammation in vivo.As it's known,inflammation plays an important role in the development and progression of atherosclerosis and cardiovascular disease.The relationship and mechanism between hs-CRP and atherosclerosis will be described in this article.

Abstract:Athrosclerosis is the risk factor of the heart and brain vascular disease.We aid to explore the part development research of athrosclerosis in order to prevent the heart and brain disease by cutting the athrosclerosis.

Abstract:Apolipoprotein mimetic peptides that mimic the function of apolipoprotein with or without bearing the sequence homology to apolipoprotein have become a hot topic of atherosclerosis therapy research.The importance of apolipoprotein mimetic peptides in atherosclerosis and related disease was established by testing in animal models,and its potential usefulness in humans has been confirmed in preliminary studies.In this article,the development of apolipoprotein mimetic peptides is reviewed.