Abstract:Aim Phosphorylation and nuclear translocation of extracellular signalregulated kinases(ERK1/2) are most important for proliferation of oxidativestressed vascular smooth muscle cells(VSMC) and heat shock protein 90(HSP90) is involved in this process.We investigate whether heat shock protein 90 participated in extracellular signal-regulated kinases 1/2 pathway as a molecular chaperon. Methods Exposure vascular smooth muscle cells to LY83583(6-Anilinoquinoline-5,8-quinolinedione,produce reactive oxygen species,1 μmol/L) for different time,then heat shock protein 90,extracellular signal-regulated kinases 1/2 and phospho-extracellular signal-regulated kinases 1/2 in cell lysates were measured by western blot.Vascular smooth muscle cells were incubated with geldanamycin (a special inhibitor of heat shock protein 90,5 μmol/L) or vehicle for 30 min,then with LY83583(1 μmol/L) for 120 min,heat shock protein 90 binding with extracellular signal-regulated kinases 1/2 and phospho-extracellular signal-regulated kinases 1/2 were quatified by immunoprecipitation and western blot.The nuclear translocation of phospho-extracellular signal-regulated kinases 1/2 were measured by immunofluorenscense. Results Heat shock protein 90 increased in a time-dependent manner.It got the peak at 120 min which corresponded to the second peak of phospho-extracellular signal-regulated kinases 1/2.Immunoprecipitation and western blot analysis showed that LY83583 increased the complex of heat shock protein 90-phospho-extracellular signal-regulated kinases 1/2 about 5.5 times(p<0.01) vs control,and phospho-extracellular signal-regulated kinases 1/2 in total cell lysis(about 6.1 times vs control,p<0.01) and nuclear increased too.Geldanamycin attenuated the effect of LY83583. Conclusions Heat shock protein 90 bound with phospho-extracellular signal-regulated kinases 1/2 and promoted their nuclear translocation in oxidative-stressed vascular smooth muscle cells.

Abstract:Aim To investigate the effects of sirolimus on proliferation and differentiation of rat smooth muscle progenitor cells(SPC). Methods Total mononuclear cells(MNC) were isolated from marrow of rats by Ficoll density gradient centrifugation method,and then plated on fibronectin-coated culture dishes. Fresh isolated MNC were treated with sirolimus(0.01～100 μg/L) or vehicle control for 12 days.SPC were characterized as adherent cells positive for α-SMA by indirect immunofluorescent staining.After 8 days cultured,attached cells were treated with sirolimus(to make a series of final concentrations: 0.1～200 μg/L) or vehicle control for 24 h.The proliferation and migration of SPC were assayed with MTT and modified Boyden chamber assay respectively.SPC adhesion assay was performed by replating those on fibronectin-coated dishes and counting the adherent cells. Results Sirolimus potently inhibited SPC outgrowth.The number of SPC at 12th day was dramatically decreased by sirolimus.At a concentration as low as 0.1 μg/L,sirolimus significantly reduced(70.9±4.5)% of SPC compared with control(p<0.01).In addition,sirolimus also inhibited SPC proliferative,migratory and adhesive capacity in a concentration-dependent manner. Conclusion Sirolimus could inhibit the proliferation and differentiation of rat smooth muscle progenitor cells.

Abstract:Aim To investigate the effect of RNA interference targeting survivin on the the intimal hyperplasia(IH) in vein graft in rats. Methods Autogenous vein graft model was established in 48 Wistar rats,transplanting the interior jugular vein to common jugular artery by microsurgical technique.The rats were divided into 4 groups according to different processing methods,including control team,empty vector team,shRNA control team and shRNA targeting surviving team.Vein graft samples were harvested on 1 or 2 weeks after surgery and survivin mRNA were measured by reverse transcription polymerase chain reaction(RT-PCR). Western blotting and immunohistochemistry were also used to detect the expression of survivin and proliferation cell nuclear antigen(PCNA).Apoptosis of vascular smooth muscle cells(VSMC) was dectected by TUNEL.IH was compared at the same time. Results The IH was evident 1 or 2 weeks after vein grafting,and ameliorated by transfection of shRNA vector of survivin(p<0.05).The expression of survivin mRNA was also inhibited significantly by shRNA of survivin.Expression of survivin and PCNA decreased greatly in shRNA team,but the positive cells of TUNEL increased significantly. Conclusion Local transfection of shRNA expression vector targeting survivin can inhibit the IH after vein graft,which maybe accomplished by the inhibition of gene and protein expression of survivin.

Abstract:Aim To investigate the effects of leptin on the migration and proliferation of vascular smooth muscle cell(VSMC) in vitro. Methods The smooth muscle cells at passage of 4～6 were incubated with leptin in different concentrations(0,20,40,80,100,200 μg/L) for 24 hours,then modified Boyden's experiment was used to measure the effect of leptin on migration;MTT was used to measure the dosage-effect curve of leptin on the growth of VSMC;and flow cytometry(FCM) was used to measure the effect of leptin on the cell cyclin. Results The growth of VSMC was promoted with the concentration of leptin,and reached the maximum(OD:0.193±0.010) at 100 μg/L,so did the effect of leptin on the proliferation index of VSMC.Leptin can promote the migration of VSMC,and the number of migrated cell was promoted with the increase of leptin concentration. Conclusion Leptin can promote the migration and proliferation of VSMC in vitro,which explicits the effects of leptin in the atherosclerosis.

Abstract:Aim To study the protective effect of imidapril on cardiac function and mitochondrion of rats with diastolic heart failure. Methods 30 SD rats were randomly divided into 5 groups:control group, DHF group,A1.5mg,A3mg,and A6mg group.DHF model was produced by abdominal aortic coarctation in the rats in the operating group.The rats in A1.5mg-A6mg groups were given with imidapril [1.5,3,and 6 mg/(kg·d)] by intragastric administration for 4 weeks,the others were treated with equal isotonic NaCl.After 4 weeks,cardiac function and hemorheology was assessed by echocardiography and catheterization.Specimens were taken and ventricular mass were measured.The level of malonaldehyole(MDA),superoxidedismutase(SOD),and glutathioneperoxidase(GSHPx) were detected by spectrophotometer.Ultra structure changes in myocardium were observed under electrion microscopy. Results In DHF group,PW,IVS,LVM,E/A ratio,SBP,DBP,LVSP,LVEDP,and MDA were increased,Tau was prolonged,LV-dp/dtmax,SOD and GSHPx was decreased.The myocardium damage including abnormality of myofilament arrangement,mitochondrial swelling and vacuolization were showed.Compared with DHF group,increased E/A ratio,IVS,PW,LVM,SBP,DBP,LVSP,LVEDP and MDA were decreased,prolonged Tau was shorted,decreased LV-dp/dtmax,SOD and GSH-Px were increased in treated groups.The myocardium damage was ameliorated in treated groups too.The protective effect of Imidapril on heart was increased according to the increasing dose of it. Conclusion Imidapril improve cardiac function in rats with DHF by ameliorating the damage of myocardic cell and mitochondrion.

Abstract:Aim To examine the effects of Ciglitazone on the expressions of intercellular adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which were upregulated by AngⅡ. Methods Human umbilical vein endothelial cells(hUVEC) at passage 35 were pre-incubated for 24 h with Ciglitazone(0.1 μmol/L,1 μmol/L,10 μmol/L,and 100 μmol/L) before stimulated by 10-7 mmol/L AngⅡ for 12 h.Total RNA was extracted,and the expression of mRNA and protein of ICAM-1 and VCAM-1 was assessed by RT-PCR and Western Blot respectively. Results Ciglitazone at 0.1 μmol/L～100 μmol/L significantly attenuated the AngⅡ-induced expression of VCAM-1(0.1 μmmol/L p<0.01,the others p<0.001) both in mRNA and protein level.Ciglitazone(0.1 μmol/L,1 μmol/L) have no effects on the expression of ICAM-1(p<0.05),but inhibited the Ang Ⅱ-induced expression of ICAM-1 at 10 μmol/L or 100 μmol/L(p<0.01,p<0.001). Conclusions Pretreatment of Ciglitazone could inhibit AngⅡ-induced the expression of VCAM-1 and ICAM-1.These findings suggest that PPARγ agonist,currently used in treatment of type Ⅱ diabetes,may have beneficial effects in modulating inflammatory response in atherosclerosis.

Abstract:Aim To observe the role of macrophage migration inhibitory factor(MIF) in proliferation of the human vascular endothelial cell line,EAhy926,cultured in vitro and the angiogenesis assay in vitro and vivo to prove that MIF could promote neovascularization. Methods Endothelial cell proliferation promoted by MIF was detected by MTT colorimetric assay.Angiogenesis in vitro was detected by ECMatrix gel,a numerical value was associated with a degree of angiogenesis progression.Angiogenesis in vivo was detected by the factorⅧ immunohistochemical staining,with injecting the matrigel plug in BALB/c Mice. Results MIF could promote the human endothelial cell proliferation,stimulate the tube formation of endothelial cells in vitro,and promote the b1ood vessels formation in matrigel plug in vivo. Conclusion Macrophage migration inhibitory factor plays a specific role in promoting neovascularization.

Abstract:Methods 50 animals were randomly divided into five groups(n=10 in each): control group(A),MIR group(B),MIR+LGT group(C),MIR+L-Arg group(D),MIR+LGT+L-Arg group(E).The mitochondrial respiratory function,Ca²⁺ concentration(m),malondialdehyde(MDA) content and superoxide dismutase(SOD) activity were determined.Meanwhile,the contents of ATP and EC in the myocardial tissue were measured,respectively.Results It was found that mitochondrial respiratory control rate(RCR),state 3 (ST3),SOD,ATP and EC levels of myocardial tissue in C,D,E group were higher than those of B group,but state 4(ST4),m,MDA were lower.However,between E and A group,all parameters had no significant differences.Conclusion LGT and L-Arg can improve function of mitochondria in myocardial cells in the reperfusion injury after myocardial ischemia by decreasing oxygen free radical level and Ca²⁺ overload in the mitochondria.

Abstract:Aim To examine the effect of rapamycin on reducing neointima formation and the proliferition of vascular smooth muscle cell(VSMC) after local application of rapamycin in a mouse model of vein graft. Methods Vein graft model was established in 30 Wistar mice which were randomly divided into two groups: rapamycin group and control group.In the rapamycin group,200 μg of rapamycin was applied locally.The control group did not receive local treatment.Graft veins were harvested 4 weeks later and underwent morphometric analysis as well as immunohistochemical analysis. Results Morphometric analysis indicate that the thickness of neointima in rapamycin group is obviously less than that in control group(13.8±0.6 μm vs 36.4±1.6 μm,p<0.05).Immunohistochemical analysis shows that the reduction of bcl-2 positive cells in vascular smooth muscle of rapamycin group was 16.6%±2.2% vs 51.3%±3.4%(p<0.05) and the decreased amount of bax positive cell was 63.3%±3.2% vs 16.3%±1.3%(p<0.05). Conclusion Local application of rapamycin can inhibits restenosis in experimental vein graft.

Abstract:Aim To approach the change of platelet activation before and after stenting for coronary artery disease and the relationship among stable angina pectoris(SAP),unstable angina pectoris(UAP),acute myocardial infarction(AMI),number of stent implantation and platelet activation. Methods Detection of positive expression of platelet membrane glycoprotein CD62p,CD63 and thrombin-sensitive protein(TSP) was performed by flow cytometry and monoclonal antibody in 175 patients.They were divided into four groups: SAP group(48 patients with stable angina);UAP group(45 patients with unstable angina);AMI group(37 patients with acute myocardial infarction) and control group(45 patients with angiography). Results There were increased the levels of CD62p,CD63 and thrombin-sensitive protein expression after stent implantation in coronary artery disease(p<0.01),and the expression levels of UAP group and AMI group were higher than that of control group(p<0.01).The positive expression of CD62p,CD63 and thrombin-sensitive protein were related to number of stenting. The more stenting,the higher positive expression. Conclusion Unstable angina and acute myocardial infarction presented high level of platelet activation,atherosclerosis plaque rupture and prone to thrombosis.Stenting induced endothelial damage augmented platelet activation and increased the risk of thrombosis.

Abstract:Aim To study the effect of basic fibroblast growth factor(bFGF) on inducing cardiac microvascular endothelial cells(CMEC) to form new blood vessels and the role of vascular endothelial growth factor receptor-1(VEGFR-1,Flt1). Methods Mouse CMEC were isolated and cultured.CMEC was induced to develop tube structure by using Matrigel so as to detect the influence of bFGF on neovascularization.Reverse transcription polymerase chain reaction(RT-PCR) assayed the expression of Flt-1mRNA. Results CMEC can be induced to develop tube structure by Matrigel in vitro.The number of vessel gradually increased with the concentrations of bFGF step up(0,5,10,20 μg/L) and decreased when bFGF was 40 μg/L(p<0.05).The expression of Flt-1mRNA gradually increased with the concentrations of bFGF step up(0,5,10,20 μg/L) and decreased when bFGF was 40 μg/L(p<0.05). Conclusion Mouse CMEC can be induced to develop tube structure by Matrigel in vitro.Mouse bFGF can promote CMEC to form new blood vessels and in certain rage show a dose-dependent manner.bFGF can enhance the expression of Flt-1 and in certain rage show a dose-dependent manner;this dose-dependent manner is similar to that of new blood vessels' quantity.

Abstract:Aim To investigate the protective effect of grasp seed procyanidins (GSP) on homocysteine(HCY)-induced cell viability in human umbilical vein endothelial cell(HUVEC) and related molecular mechanisms. Methods Cell viability was analyzed by using MTT and lactate dehydrogenase(LDH) assay.The levels of superoxide dismutase(SOD),glutathione peroxidase(GSHPx) and malondialdehyde(MDA) were examined by kits and the level of intracellular reactive oxygen species(ROS) were determined by flow cytometric assay.Proteins and phosphorylation levels were examined by Western blot. Results Treatment of cultured HUVEC with HCY for 48 hours induced a significant decrease of cell viability.The levels of intracellular ROS and MDA were enhanced,and the activities of SOD and GSHPx were decreased.However,simultaneous treatment with GSP exhibited cytoprotective effects,reduced formation of the MDA and ROS,maintained the activity of SOD and GSHPx,prevented the phosphorylation of exrtacellular signal regulated kinase(ERK),p38 and c-Jun N-terminal kinase(JNK). Conclusion These results demonstrated that GSP had the protective capacity to antagonize HCY induced cell toxicity in HUVEC.The protective effect of GSP may be partially dependent on an anti-oxidative stress effects and then inhibition of the activation of mitogen-activated protein kinase(MAPK).

Abstract:Aim To investigate the change of Cysteine-rich 61 in rats abdominal artery injured by balloon. Methods Forty-eight Wistar male rats were studied.Balloon injury was conducted in abdominal artery respectively.Rats were killed at different time points and abdominal artery were collected in time.Intimal hyperplasia was studied by histological morphology method.The expression of tissue Cysteine-rich 61 was determined by immunohistochemically,reverse transcription polymerase chain reaction and western-blot. Results Intimal hyperplasia was present at 7th day after balloon injury,became more obvious at 14th day and in progression at 28th day.No change was observed in control group.The expression of Cysteine-rich 61 increased significantly at 7th day and 14th day after balloon injury,and it was significantly different between injury group and control group(p<0.01).The expression of Cysteine-rich 61 was not significantly different between injury group and control group at 28th day(p<0.05). Conclusions Cysteine-rich 61 expressed stronger in injury group than that in control group,which indicated that Cysteine-rich 61 may play an important role in intimal hyperplasia caused by balloon injury.

Abstract:Aim To observe the effects of monocyte chemotactic protein-1(MCP-1) and Fractalkine on tissue factor(TF) expression,proliferation and chemotaxis of vascular smoth muscle cell(VSMC). Methods The effects of MCP-1,Fractalkine and MCP-1+Fractalkine on TF antigen expression were analyzed by enzyme linked immunosorbent assay(ELISA).Their effects on VSMC proliferation were analyzed by MTT.And their effects on VSMC chemotaxis were evaluated by cell chemotaxis experiment. Results MCP-1 or Fractalkine could induce TF antigen in VSMC,but was less effective by MCP-1+Fractalkine than by MCP-1 or Fractalkine.MCP-1 and Fractalkine had competitive inhibition.Fractalkine had a strong impact on VSMC proliferation,while MCP-1+Fractalkine or MCP-1 had not.Fractalkine and MCP-1+Fractalkine induced the VSMC chemotaxis,while MCP-1 had little such function. Conclusions MCP-1 and Fractalkine had important effects on the atherosclerosis by working on TF expression,VSMC proliferation and chemotaxis.

Abstract:Aim To study the relationships of methylenetetrahydrofolate reductase(MTHFR) gene C677T polymorphism with essential hypertension and arterial compliance. Methods Genotype of MTHFR gene C677T polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) analysis and characterized by electrophoresis and sequencing in 695 patients with essential hypertension and 509 age-matched normal controls.Carotid-radial pulse wave velocity(C-R PWV) and carotid-femoral pulse wave velocity(C-F PWV) was performed. Results In essential hypertension group,the frequencies of TT genotype and T allele were significantly higher than those of control group(26.5% vs 20.6% and 48.7% vs 42.4%,P=0.015 and 0.002).The C-F PWV of people with T allele was markedly higher than that of people with CC genotype(p<0.05),and the C-R PWV of hypertensive patients with T allele was also higher than that of with CC genotype(P=0.001).The C-F PWV of isolated systolic hypertension(ISH) patients with T allele and the C-R PWV and C-F PWV of no isolated systolic hypertension(NISH) patients with T allele were significantly higher than those of patients with CC genotype(p<0.05). Conclusion MTHFR C677T gene polymorphism may be related to increased risk of essential hypertension,and the 677T allele in MTHFR may be a genetic factor of arterial stiffness in hypertensive patients.

Abstract:Aim To examine the advanced oxidation protein products(AOPP) and malondialdehyde(MDA) in patients with acute coronary syndrome(ACS) and discuss the relationship between oxidative stress and the development of atherosclerosis(As). Methods Plasma were collected in 73 acute myocardial infarction(AMI) patients including 46 patients undergone selective percutaneous coronary intervention(PCI)and 27 patients undergone emergency PCI,49 unstable angina pectoris(UAP) patients and 21 non-coronary artery disease(non-CAD) patients.All cases were undergone coronary angiography(CAG).Plasma were collected immediately,post-24 hours and post48 hours after patients were recruited.AOPP were determined by measurements of optical density(OD) via spectrophotometry,and MDA was measured with TBA methods. Results Compared with normal group(without CAD),plasma AOPP were significantly higher in AMI(selective PCI) and UAP patients(p<0.05).Significant difference also existed between selective PCI group and emergency PCI group in AMI patients (p<0.01).AOPP levels of UAP patients were significantly decreased after 48 hours(p<0.05);Pearson correlation analysis showed that AOPP was positively correlated to low density lipoprotein cholesterol(LDLC) in AMI patients(p<0.01).Compared with normal group(without CAD),plasma MDA were significantly higher in all AMI patients(p<0.05). Conclusions Oxidative stress may be an important step in development of ACS.AOPP and MDA may be as good markers in ACS patients.

Abstract:Aim To investigate the protect function of clopidogrel on blood vessel endothelium in patients with coronary heart disease(CHD). Method 166 patients with CHD confirmed by coronary arteriography were randomly divided into two groups.At the first six months the two groups were all treated with clopidogrel and aspirin.At the last six months the control group were only treated with aspirin and the case group continued with clopidogrel and aspirin(other foundation medicine in CHD were the same at the two groups).Compliance and endothelial function of brachial artery were determined by pulsed Doppler technique at 6th month and 12th month.Brachial artery diastolic diameter(Dd),mean flow velocity(Vm),blood flow volume(Q),distensibility(DC),resistance of blood flow(R) and intima-media thickness(IMT) were used as the indexes of compliance of brachial artery.While the brachial artery diastolic diameter(Dd'),the mean flow velocity(Vm'),the blood flow volume(Q') and the resistance of blood flow(R') after brachial artery reactive hyperaemia were used as the indexes of endothelial function of it. Results At the case group,the brachial artery diastolic diameter,mean flow velocity,blood flow volume and distensibility increased,resistance of blood flow and IMT cut down,and there were significant changes in 12th month vs 6th month.There were significant changes between the case group and the control group in improving the function of blood vessel endothelium at 12th month.At the case group,the brachial artery diameter,flow velocity,blood flow volume increased in artery reactive hyperaemia test and resistance of blood flow cut down.At the control group,the brachial artery diameter,blood flow volume and resistance of blood flow did not change in 12th month vs 6th month. Conclusion Long-term treatment with clopidogrel may improve the compliance and endothelial function of blood vessel endothelium.

Abstract:Aim To investigate the intervenient efficacy of simvastatin and aspirin as well as blood sugar controlling therapy for carotid arteriosclerosis in patients with type 2 Diabetes. Methods 158 patients with type 2 diabetes and carotid arteriosclerosis were randomized into two groups.80 cases in the treatment group,were treated with both simvastatin and aspirin as well as hypoglycemia drugs;while 78 cases in the control group were treated with hypoglycemia drugs alone.Intima-media thickness(IMT) and internal diameter of Carotid arterial,the IMT and internal diameter ratio,carotid plaques score,glucose levels and the levels of serum lipids and were measured before and once a year after treatment for 3 years. Results Mean IMT of carotid artery and carotid plaques score were 1.02±0.11 mm and 3.8±2.4 respectively in the treatment group 1 year after treatment,showed no difference from that before treatment.But they were 0.89±0.15 mm and 2.7±1.6,0.89±0.14 mm and 2.5±1.1 after 2 and 3 years respectively,which were reduced significantly compared with that before treatment.The IMT and internal diameter ratio was also reduced significantly after treatment.Overall incidence of cardio-and cerebro-vascular events in the treatment group were 3.75% and 10.00% during the 3 years follow-up period,which were significantly lowed compared to the control group. Conclusions Long-term simvastatin and aspirin theraty could effectively delay and reverse the progression of carotid arteriosclerosis in patients with type 2 diabetes and prevent cardio-and cerebro-vascular events when combined with hypoglycemia drugs.

Abstract:Aim To study the relationship between serum androgen and atherosclerosis in males. Methods 134 male patients in hospital were divided into four groups according to the result of coronary arteriography: single vessel disease group(n=30),double vessel disease group(n=33),triple vessel disease group(n=28),and the control group(n=43).Serum total testosterone(TT),free testosterone(FT),dehydroepiandrosterone(DHEA),serum total cholesterol(TC),triglycerides(TG),low density lipoprotein cholesterol(LDLC),high density lipoprotein cholesterol(HDLC),lipoprotein a(Lpa),fasting blood glucose(FBG),fasting insulin(FIN) level,homeostasis modle assessment insulin resistance(HOMA-IR) and intima-media thickness(IMT) of the carotid wall were detected in all patients. Results Compared with the control group,the coronary artery disease(CAD) group had significantly decrease in serum FT,HDLC(p<0.001) and significantly increase in serum TC,LDLC,Lpa,FIN,HOMA-IR,FBG and IMT(p<0.05).Serum FT was higher in control group than in CAD group(p<0.001);IMT was lower in control group than in each CAD subgroups(p<0.001).As for serum FIN and HOMA-IR,there were significantly differences between control group and CAD subgroups(p<0.001).Serum FBG was significantly lower in control group than in triple vessel disease group(p<0.01).In Pearson relative analysis,IMT had obvious negative correlation with serum FT,HDLC(r<-0.5,p<0.001),while positive correlation with serum FIN,LDLC,and Lpa(r>0.5,p<0.001). Conclusion The IMT in patients with CAD was thicker than that in control group.The serum FT level in men with CAD was obviously lower than that with normal coronary artery.FT may play roles in the formation of the coronary atherosclerosis in males by influenceing the blood lipoprotein,blood glucose and the resistance of the insulin.

Abstract:Aim To study the association of TaqIB polymorphism of the cholesteryl ester transport protein(CETP) gene in Chinese population via meta analysis. Methods Case-control studies published before 31 Dec.2005 about the association of CETP gene TaqIB polymorphism and coronary artery disease in Chinese population were searched in three digital databases including CBMdisc,CHKD and Medline. All the literatures were evaluated and abstracted based on the defined selection criteria by two independent investigators.Publication bias was tested by funnel plot and the odd ratios of all studies were combined dependent on the result of heterogeneity test among the individual studies.The software Review Manager (Version 4.2) was used for meta analysis. Results Seven studies containing 1 161 patients with coronary artery disease and 1 149 control subjects were analyzed. There was no publication bias in 7 reviewed studies,heterogeneity test of reviewed studies showed that there was no significant statistic differences(χ2=3.53,P=0.74) among the OR of individual studies. The summarized odds ratio of coronary artery disease for B1B1 genotype versus B1B₂ and B₂B₂ genotypes across all 7 studies was 1.34(95% CI: 1.12～1.60,P=0.002). Conclusion In Chinese Han nationality,the TaqIB polymorphism in CETP gene is associated with susceptibility of coronary artery disease and the allele B1 might be a genetic risk factor for coronary artery disease.