Abstract:Aim To observe the effects of simvastatin on nuclear factor-κB(NF-κB)-DNA binding activity and on the expression of matrix metalloproteinase(MMP)-1 and 3 in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Methods Thirty-six New Zealand male rabbits were randomly divided into low cholesterol group(LC),high cholesterol group(HC),high cholesterol+simvastatin group(HC+S),and then were fed for 12 weeks.At the end of experiment,standard enzymatic assay,electrophoretic mobility shift assay(EMSA),immunohistochemistry staining,and morphometry were performed to observe serum lipids,NF-κB-DNA binding activity,MMP-1 and 3 protein expression,intima thickness and plaque area of aorta respectively in all three groups. Results The serum lipids,NF-κB-DNA binding activity,expression of MMP-1 and 3 protein and intima thickness of aorta in the LC group and HC+S group were significantly lower than those in the HC group(p<0.05).There was no significant difference in the serum lipids between the LC group and HC+S group(p<0.05),but the NF-κB-DNA binding activity,the expression of MMP-1 and 3 protein and the intima thickness of aorta in the HC+S group were significantly decreased compared with the LC group(p<0.05). Conclusions This study demonstrates that simvastatin could inhibit the NF-κB-DNA binding activity,reduce the expression of MMP-1 and 3 protein,and decrease atherosclerosis.

Abstract:Aim To investigate the effect of peroxisome proliferator-activated receptor γ(PPARγ) ligands on inflammatory cytokine and matrix metalloproteinase(MMP) secretion by macrophages and foam cell. Methods THP-1 monocytes were differentiated to macrophages in vitro by addition of PMA,and then induced into foam cell by oxidized low density lipoprotein(ox-LDL).Semi-quantitative reverse transcription polymerase chain reaction(RT-PCR) was performed to detect the expression of PPARγ.Macrophage CD40 protein expression was detected by Western blot.Interleukin 6(IL-6),tumor necrosis factor α(TNF-α) and MMP-9 secretion in foam cell culture medium was measured by enzyme-linked immunosorbent assay(ELISA).MMP-9 activities were determined by gelatin zymography. Results Macrophages expressed PPARγ and treatment with ox-LDL did not affect the expression.PPARγ ligand pioglitazone greatly inhibited macrophage expression of CD40 in a dose-dependent manner.Moreover,pioglitazone significantly inhibited the secretion of IL-6,TNF-α and MMP-9 by foam cell as well as the activity of MMP9(p<0.05),although it had no effect on MMP-2 secretion or activity. Conclusions peroxisome proliferator-activated receptor γ ligands significantly inhibited the secretion of several inflammatory molecules by macrophages/foam cell which were closely related to atherosclerotic (As) plaque development and plaque instability.Thus,PPARγ ligands may have potential advantages in As therapy.

Abstract:Aim To investigate the effects of tissue factor(TF) on the expression of macrophage inflammatory protein-in-1α in cultured human umbilical endothelial cell(hUVEC). Methods Different concentrations of tissue factor were incubated with hUVEC.Cell enzyme linked immunosorbent assay(ELISA) was used to detect the expression of ma(rophage inflammatory protein-1α.Monocyte adhesion assay was used to detect the monocyte adhesion.ma(rophage inflammatory protein-1α mRNA expression were determined by reverse transcriptase-polymerase chain reaction(RT-PCR). Results Tissue factor dramatically enhanced the levels of ma(rophage inflammatory protein-1α in a dose dependent manner,increasing ma(rophage inflammatory protein-1α protein expression in hUVEC by 127%±14% at 0.01 nmol/L,151%±11% at 0.10 nmol/L,196%±13% at 1.00 nmol/L and 267%±43% at 10.00 nmol/L.In addition,10.00 nmol/L of TF for 2 hours could significantly increase the amount of monocyte adherence to endothelial cell.Moreover,RT-PCR analysis demonstrated that the amount of ma(rophage inflammatory protein-1α mRNA was increased after treatment withTF for 24 hours. Conclusion Tissue factor can induce ma(rophage inflammatory protein-1α expression in hUVEC,which may thereby influence the pathogenesis of atherosclerosis.

Abstract:Aim To study the effects of late reperfusion on cardiocyte apoptosis and the expression of bcl-2 and bax mRNA and related proteins in the risk areas after acute myocardial infarct in dogs. Methods After chest was opened and the coronary artery was exposed,twenty eight dogs were randomly divided into three groups: sham operation group(n=8),acute myocardial infarction group(n=10),and late reperfusion group(n=10).Apart from sham operation group,the left anterior descending arteries were occluded for 12 h in acute myocardial infarction group and 6 h occlusion followed by 6 h of reperfusion in late reperfusion group.The cardiocyte apoptosis was measured by TUNEL assay,the expression of bcl-2 and bax gene mRNA by RT-PCR.Immunohistochemistry and Western blot analysis were used to detect the expression of bcl-2 and bax protein. Results The apoptotic index of cardiocyte in late reperfusion group was much higher than that of sham operation group(p<(0.01)),but less than that of acute myocardial infarction group(p<0.05).Compared with sham operation group,the expression of bcl-2 mRNA and protein were significantly increased in acute myocardial infarction group and late reperfusion group(p<(0.01)),and there were no significant difference between acute myocardial infarction group and late reperfusion group(p<0.05).The expression of bax mRNA and its protein in late reperfusion group was much higher than that of sham operation group(p<0.01), but lower than that of acute myocardial infarction group(p<0.05). Conclusions Late reperfusion of infarct-related artery can decrease cardiocyte apoptosis in the risk area of acute myocardial infarction,which may be related to the reduction of the expression of bax mRNA and protein.

Abstract:Aim To observe the protein expression of cyclophilin A in lipid-loaded macrophages induced by oxidized low density lipoprotein(ox-LDL) and its effect on cellular cholesterol accumulation. Methods RAW264.7 mouse macrophages were treated with 75 mg/L ox-LDL for 0,24,48 and 72 hours.Oil red O dye experiment was used to show the lipid droplets in lipid-loaded macrophages. High performance liquid chromatography(HPLC) analysis was peformed to determine the content of cellular total cholesterol(TC) and cholesterol ester(CE).Westernblot analysis was used to detect the protein expression of cyclophilin A.Then,75 mg/L Probucol was added in the cells treated with ox-LDL for 48 hours. Results With ox-LDL treatment after 48 hours,Oil red O dye showed a lot of lipid droplets accumulated in RAW264.7 macrophages,HPLC analysis showed the content of cellular TC and CE were increased greatly and Western-blot analysis showed the expression of cyclophilin A was significantly decreased.However,with Probucol treatment,cyclophilin A was greatly increased,the lipid droplets significantly decreased,and the content of TC and CE also decreased. Conclusion The protein expression of cyclophilin A was down-regulated in lipid-loaded macrophages while the content of cellular TC and CE were increased greatly.However,Probucol could up-regulate the cyclophilin A expression and decrease the cellular cholesterol accumulation.

Abstract:Aim To research the hemodynamic property and the anti-calcification feature of bovine jugular vein conduit cross-linked by dye-mediated photooxidation. Methods Right ventricular outflow tract(RVOT) was reconstructed for 12 canines,7 with bovine jugular vein conduits cross-linked by dye-mediated photooxidation treatment,7 with bovine jugular vein conduits simply cross-linked by glutaraldehyde.After feeding 9 to 10 months,then the hemodynamic property was evaluated by echocardiography and heart catheter examination.Tissue calcium content was analyzed by flame atomic absorption spectrophotometer. Results Echocardiography revealed that the motion of the valvular leaflets in both groups of conduit that cross-linked by glutaraldehyde and cross-linked by dye-mediated photooxidation were satisfying.Heart catheter revealed the transvalvular pressure gradients of both studied groups were minimal.Walls of bovine jugular vein conduit that cross-linked by dye-mediated photooxidation treatment had less calcification than bovine jugular vein conduits that simply cross-linked by glutaraldehyde.Compared with the latter ones,the tissue calcium content of the formers decreased 65.6%.It is also found that the walls of the bovine jugular vein had far more calcification than the valves in both groups. Conclusions RVOT with bovine jugular vein conduits was reconstructed at 9～10 months,which hemodynamic property seems equivalent to pulmonary artery.The bovine jugular vein cross-linked by dye-mediated photooxidation treatment appears to have less calcification.

Abstract:Aim To study the effects of tetramethylpyrazine(TMP) on calmodulin(CaM) and calcinuerin(CaN) in the proliferation of vascular smooth muscle cell(VSMC) induced by angiotensinⅡ(AngⅡ). Methods A cell proliferating model of VSMC induced by angiotensinⅡ(AngⅡ) was established;the varity of CaM and CaN activities affected by tetramethylpyrazine(TMP) at different time and different concentration was observed by enzyme reaction phosphorus measurement. Results Cell proliferation activity,CaM and CaN activities were increased significantly in VSMC proliferation induced by AngⅡ(p<0.01).While treated with TMP,the index were obviously reduced compared with AngⅡ group(p<0.01). Conclusions The VSMC proliferation induced by AngⅡ can be inhibited by TMP significantly,and the inhibiting mechanism of TMP may be related to inhibiting CaM and CaN activities then restraining the proliferation of VSMC in a dose and time-dependent manner.

Abstract:Aim To investigate the relationship between tetrandrine(Tet) on prevention and treatment of restenosis and phenotypic modulation of vascular smooth muscle cells(VSMC) as well as its signal transduction pathway after vascular intimal injury. Methods HE staining was used to analyse vascular morphology change at sham-injured,injured and Tet-treated group 28 days.Immunohistochemistry and Western blot were respectively used to detect the expression change of smooth muscle α-actin(SM α-actin) and proliferation cell nuclear antigen(PCNA),p38 in injured group and Tet group at 7,14 and 28 days after balloon injury. Results The every layer structure in vascular wall of sham-injured artery was intact.Neointimal area was obviously increased and lumen area was notably decreased in injured group.In the Tet group the intimal proliferation was showed but notably weaker than that of the injured group and lumen area notably increased.Compared with the injured group,the expression of SM α-actin,PCNA and p38 in vascular wall of the Tet group was not significantly different and neointimal proliferation degree was also basicly the same at 7 days after injury.The expression of PCNA and p38 in Tet group was all significantly lower than that in injured group in vascular wall at 14 and 28 days after injury.However,expression of SM α-actin in Tet group was slightly higher than that in injured group at 14 days, and not significantly different between the two groups at 28 days. Conclusion Tet could reduce neointimal hyperplasia by inhibiting VSMC phenotypic modulation and its signal transduction.

Abstract:Aim To observe the effect of simvastatin on the expression of lectin-like oxidized low density lipoprotein receptor-1(LOX-1) mediated by oxidized low density lipoprotein(ox-LDL) in cultured human umbilical vein endothelial cells(hUVEC,ECV304). Methods ECV304 Cells were divided into several groups in random: control,LDL(25 mg/L),ox-LDL(25,50 and 100 mg/L) and ox-LDL(50 mg/L)+simvastatin(1 and 10 μmol/L).Then LOX-1 mRNA expression was detected by reverse transcription-polymerase chain reaction(RT-PCR),and LOX-1 protein expression was detected by Western blot. Results Ox-LDL markedly induced the increase of cells LOX-1 mRNA and protein expression(p<0.01),and the increase of LOX-1 was dependent on ox-LDL concentration(p<0.05).Simvastatin reduced ox-LDL induced expression of LOX-1(p<(0.05)),and the high concentration of statins was more potent than the low concentration(p<0.05). Conclusions These observations indicate ox-LDL results in endothelial dysfunction and atherosclerosis by LOX-1.The function of statins on reducing ox-LDL-mediated LOX-1 expression may be one of the mechanisms of anti-atherosclerosis,independent of cholesterol-lowering effect.

Abstract:Aim To observe the anti-atheromatous effects of fenofibrate in cholesterol-fed rabbits. Methods 10 male New Zealand white rabbits were fed with high cholesterol diet for 8 weeks,and then were randomly divided into two groups: high cholesterol group maintained cholesterol diet for 4 weeks;fenofibrate treatment group maintained the same cholesterol diet besides supplementing with fenofibrate30 mg/(kg·d)] for 4 weeks.And control group was fed with normal diet for 12 weeks.Before and after feeding,serum tumor necrosis factor-α(TNFα) levels of all rabbits were measured.After feeding,the aortas were harvested for observing the formation of atherosclerotic plaques.TNF-α mRNA expression in adipose tissue was evaluated by reverse transcription-polymerase chain reaction(RT-PCR). Results High cholesterol group and fenofibrate treatment group showed higher serum levels of total cholesterol and low density lipoprotein cholesterol than those of control group(p<0.001),but there were no difference between the two groups(p<0.05).As compared with the high cholesterol group,aortic atherosclerotic area(52.8%±6.9% vs 76.3%±8.6%,p<0.01),intimal thickness of the aorta(28.45±5.68 μm vs 76.18±11.25 μm,p<0.05),serum TNF-α levels(2.11±0.26 ng/L vs 3.86±0.33 ng/L,p<0.05) and TNF-α mRNA expression in adipose tissue (0.31±0.05 vs 0.56±0.07,p<0.05) were significantly decreased in fenofibrate treatment group. Conclusions The study indicates that fenofibrate manifests an anti-atheromatous effect independent of the hypolipidemic effect in cholesterol-fed rabbits and decreasing serum TNF-α level may be one of its possible mechanisms.

Abstract:Aim To investigate the effect of total flavone of radix puerariae on atherosclerotic plaque formation of aortic sinus in apolipoprotein E gene deficient(ApoE~(-/-)) mice. Methods 32 ApoE~(-/-) mice were divided randomly into four groups: model group,total flavone of radix puerariae low-dosage group(15 mg/kg everyday),total flavone of radix puerariae high-dosage group(85 mg/kg everyday) and atorvastatin calcium positive control group(5 mg/kg everyday).There were 8 mice in each group.The treatment group was stomach perfusion with relevant drug,the model group was stomach perfusion with equal amount of normal saline,and both group were medicated for 12 weeks and were fed with general diet.The routine biochemical method was used to measure total cholesterol,triglyceride and high-density lipoprotein-cholesterol in serum;and the serial paraffin section and Hematoxylin and eosin(HE) staining of aortic root were used to observe the histomorphological change of aortic sinus and measure the size of aortic sinus plaque in ApoE~(-/-) mice. Results A total of 65 plaques were detected in four groups.Despite the typical middle/advanced pathological changes of aortic sinus(such as fibrous plaque and/or atheromatous plaque),four groups were different in histological observation.In model group,some plaques were bigger,merged into flake,aortic wall thickened diffusively,aortic cavity was narrower.In otal flavone of radix puerariae treatment group and atorvastatin calcium positive control group,the aortic sinus had a more limited plaque lesion and a slighter narrowing of aortic cavity. The ratio of plaque area to aortic cavity area was significantly smaller in total flavone of radix puerariae high-dosage group,total flavone of radix puerariae low-dosage group and atorvastatin calcium positive control group than that in model group,and was significantly smaller in total flavone of radix puerariae high-dosage group than that in total flavone of radix puerariae low-dosage group(p<0.01). Conclusions Total flavone of radix puerariae can inhibit to some extent the progress of atherosclerotic plaque in ApoE~(-/-) mice,which might not be significantly related to its effect of decreasing mice blood lipid.

Abstract:Aim To construct the recombinant adeno-associated virus vector(rAAV) expressing the human tissue kallikrein(HK) gene and detect the expression of interested gene in human umbilical vein endothelial cell(hUVEC) which were infected with different titer of rAAV.The feasibility of gene therapy for hypertension by rAAV mediated human tissue kallikrein gene transfection was discussed. Methods The HK gene was directionally cloned into the pAAV-MCS,and co-transfected AAV-293 cell with other two plasmids(the pAAV-RC,and pHelper) by lipofectamine.The recombinant AAV particles were harvested and the viral titer was measured.Then hUVEC were infected with different titer of rAAV particles.72 hours later,the expression of human tissue kallikrein gene was detected by RT-PCR and ELISA. Results The AAV expressing system of human tissue kallikrein gene was successfully constructed with a titer of 6.2×10~(10) particles/L measured with In Situ β-Galactosidase Staining Kit.Compared with control group,the expression of HK gene in groups infected with rAAV at different titer of 1×10~9,1×10~8,1×10~7 increased significantly(p<0.05),especially in the group of 1×10~9(p<0.001). Conclusions When co-transfecting AAV-293 cell with three plasmids(the recombinant pAAV expression plasmid,pAAV-RC,and pHelper),the titer of rAAV particles can reach >10~(10) particle/L stably.The interested gene can be expressed significantly and stably when using recombinant AAV viral to infect the cultured mammal cell.

Abstract:Aim To investigate the effects of losartan on oxidative stress and the contents of vascular smooth muscle cells(VSMC) and macrophages in aortic atheromatous plaques of apolipoprotein E gene-deficient(Apo E~(-/-)) mice. Methods Twenty seven Apo E~(-/-) mice were randomly divided into three groups: control group,low dose losartan group5 mg/(kg·d)] and high dose losartan group25 mg/(kg·d)].The period of administration was 20 weeks.Serum nitric oxide(NO),superoxide dismutase(SOD),malondialdehyde(MDA)and serum lipids were measured by routine biochemical method.Aortic paraffin slice were prepared for histomorphological observation.The contents of VSMC and macrophages were detected by immunological histochemical method. Results There were no significant difference in serum lipids among three groups.Comparing with the control group,serum NO levels of the two treatment groups were significantly increased(p<0.01),the activity of SOD was notably enhanced(p<0.01),content of MDA was markedly decreased(p<0.05 and p<0.01).There were also significant differences between the two treatment groups(p<0.01).The atheromatous plaques of the two treatment groups contained some thick fibrous caps and little lipid cores.The contents of VSMC in the two treatment groups were significantly higher than that of control group(p<0.01).On the contrary,macrophages were notably lower than that of control group(p<0.01).Meanwhile,there were also significant differences between the two treatment groups(p<0.01 and p<0.05). Conclusions Without affecting the serum lipids,losartan can attenuate oxidative stress in Apo E~(-/-) mice and stabilize atheromatous plaque by means of increasing the content of VSMC and reducing macrophages.

Abstract:Aim To investigate the relationship between aquaporin-4(AQP4)mRNA expression and blood-brain barrier(BBB) permeability after experimental cerebral hemorrhage in rats. Methods The cerebral hemorrhage models were established by stereotaxic injection of auto-non-anticoagulant artery blood into the caudate nucleus.AQP4 mRNA expression was detected by RT-PCR,BBB permeability by Evens Blue method and brain water contents by dry-wet weight method. Results In contrast to the control group,AQP4 mRNA expression increased in cerebral hemorrhage group at 6 hours(1.06±0.12),reached peak at 3 days(1.34±0.14),then was still higher than normal at 7 days(p<0.05);BBB permeability increased at 6 hours after cerebral hemorrhage(0.5955±0.0956),reached peak at 1～3 days(0.8889±0.0968,0.7914±0.0520),and decreased at 5～7 days gradually(p<0.05).There was a significantly positive correlation between AQP4 mRNA expression and BBB permeability(r=0.686,p<0.01),which was consistent with the change of cerebral edema. Conclusion Cerebral edema may be formed through the upregulation of aquaporin-4 mRNA expression and the increase of BBB permeability after cerebral hemorrhage.

Abstract:Aim To study the effects of L-carnitine against ischemic/reperfusion injury in vivo rabbits cardiomyocyte and its possible mechanism. Methods Myocardial ischemic/reperfusion models were built in healthy new Zealand rabbits.Rabbits were subjected to 30 min myocardial ischemia followed by reperfusion for 3 h.Anesthetized rabbits were randomly divided into 3 groups: blank control group(n=5)in which left anterior descending coronary artery was exposed and a piece of silk thread was placed around the artery but not tied;saline control group(n=10) in which normal saline was injected into sublingual vein after MI 30 min;L-carnitine group(n=10) received intravenous Lcarnitine 3.0 g and saline 250 mL after MI 30 min.ECG throught the experiment, free fatty acid(FFA),superoxide(SOD),malonaldehyde(MDA),creatine kinase(CK),Na~+-K~+-ATPase and Ca²⁺-Mg~(2+)-ATPase were all observed after reperfusion.The content of Heart shork protein 70 obstained below ischemia/ reperfusion region 5 mm through myocardial layment was determined by western blot. Results Compared with blank control group or saline control group,L-carnitine group showed protection against MI/R injury as evidenced by more effective improvement in ST of ECG,marked increase of Na~+-K~+-ATPase,Ca²⁺-Mg~(2+)-ATPase,SOD;and marked decrease of FFA and MDA.The content of CK has tendency of decline.The content of HSP 70 was dramatically increased((p<0.05)). Conclusions L-carnitine can protect cardiomyocyte from ischemic/reperfusion injury through many aspects by inducing HSP70.

Abstract:Aim To investigate the anti-oxidation and-inflammation function of probucol in the elderly patients with low extremity atherosclerosis disease(LEASD) by measuring plasma cholesterol,oxidized low density lipoprotein(ox-LDL) and inflammation parameters before and after treatment. Methods 54 patients were divided into treatment group(n=33) and control group(n=21).Patients in the treatment group took probucol besides the routine therapy.Patients in the control group only took the routine drugs.The total treatment phase was 12 weeks.All patients did not take any lipid-lowering drugs and other anti-oxidants.Before and after the treatment,the plasma cholesterol,ox-LDL,high-sensitive C reactive protein(hs-CRP),interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α)were measured. Results After treatment,the levels of hs-CRP, IL-1β,ox-LDL and cholesterol decreased significantly(p<0.05);the differences in inflammation factors,ox-LDL and cholesterol concentration between the two groups were statistically significant(p<0.05). Conclusions Probucol could decrease the concentration of plasma cholesterol in the old patients with LEASD.Probucol could reduce the plasma level of ox-LDL,hs-CRP and IL-1β significantly,indicating its good effect of anti-inflammation and-oxidation.

Abstract:Aim To investigate whether serum levels of matrix metalloproteinase(MMP) are associated with the degree of risk in patients with acute coronary syndromes(ACS). Methods Using SDS-PAGE Zymography and Western-Blotting,Serum Pro-MMP-2,MMP-2 were measured in 78 patients ACS,28 with unstable angina(UA) and 50 with acute myocardial infarction(AMI).Control group includes 50 healthy volunteers.51 cases were in stable angina group. Results Serum MMP-2 was significantly increased in both UA(455±51 INT·mm~2)and AMI group(503±45 INT·mm~2)compared with those in control group(236±33 INT·mm~2) and stable angina(224±23 INT·mm~2)(p<0.05,respectively)by Zymography.But there was no difference between UA and AMI group(p<0.05),and there were no difference between each two subgroups of UA(which are defined low-risk,mid-risk and high-risk group) in duration time of ischemia,ECG and CK-MB/cTnI. Conclusions Increased serum level of activity MMP-2 was detected in patients with ACS.Their findings provide an insight into the unstable plaque association with MMP-2.Serum MMP-2 level appears to be a marker of plaque unstable in patient with acute coronary syndrome.

Abstract:Aim To investigate the changes of plasma soluble Fas in patients with restenosis in 6 months and effects of atorvastatin on plasma soluble Fas in patients in the early stage after percutaneous coronary intervention. Methods The levels of soluble Fas in plasma of patients were examined by means of enzyme-linked immunosorbent assay in 13 patients with restenosis,in 16 patients without restenosis in 6 months after percutaneous coronary intervention,in 20 patients with coronary artery disease,in 20 healthy without stenosis in coronary angiography,and in 20 patients treated with selective percutaneous coronary intervention and with or atorvastatin in prior percutaneous coronary intervention,6 h,24 h,3 d and 7 d after percutaneous coronary intervention. Results The levels of soluble Fas in patients with restenosis 6 months after percutaneous coronary intervention were significantly higher than those patients without restenosis,those patients with coronary artery disease and those patients without stenosis in coronary angiography(469±126 vs 132±30,123±23,43±9 ng/L,respectively,all p<0.01).The levels of soluble Fas were also significantly higher in patients without restenosis after percutaneous coronary intervention and in patients with coronary artery disease than those patients without stenosis in coronary angiography(all p<0.01).The levels of soluble Fas were rapidly increased in patients 6h after selective percutaneous coronary intervention,reached its peak after 3 d,and remained very high after 7 d. The levels of soluble Fas were significantly decreased in patients 3 d and 7 d after treatment with atorvastatin than those patients without atorvastatin(from 2 036±422 to 1 157±268 ng/L,and 1 460±266 to 798±111 ng/L,respectively,all p<0.01). Conclusions The levels of soluble Fas were significantly higher in patients with restenosis after percutaneous coronary intervention than those patients without restenosis.Persist increment of soluble Fas may act as the predictors of restenosis after percutaneous coronary intervention.The levels of soluble Fas significantly decreased after treatment of atorvastatin,which may be one of mechanisms of statins preventing restenosis that.

Abstract:Aim To observe the changes of soluble intercellular adhesion molecule-1(sICAM-1) and pregnancy associated plasma protein-A(PAPP-A) levels and to explore its clinical value combining with coronary angiography(CAG) results in patients with acute coronary syndrome(ACS). Methods The levels of serum sICAM-1 and PAPP-A were measured with enzyme linked immunosorbent assay(ELISA) in 46 patients with ACS,22 with stable angina pectoris(SAP) and 20 coronary angiography negative as controls.The results of the three groups and different numbers of diseased coronary vessels in coronary heart disease(CHD) group were analyzed. Results sICAM-1 in ACS group was significantly higher than that in SAP group(p<0.05) and control group(p<0.01),PAPP-A in ACS group was significantly higher than that in SAP group and control group(p<0.01).The sICAM-1 and PAPP-A concentrations were increased in the 1-vessel-disease group,the 2-vessel disease group,and the 3-vessel-disease group.In patients with acute myocardial infarction(AMI) and unstable angina pectoris(UAP),there were obvious correlations between sICAM-1 and PAPP-A(r=0.737,and r=0.758,p<0.001). Conclusions The levels of sICAM-1 and PAPP-A increased in ACS patients,which may reflect the instability of atherosclerotic plaques.