Abstract:Aim To investigate the effect of resveratrol on reendothelialization and intimal hyperplasia in balloon injured aorta of rat and its potential mechanism. Methods 54 healthy male Sprague-Dawley rats were randomly divided into 4 groups: sham operation group(n=9),placebo-treated group(n=15),small dose resveratrol [10 mg/(kg·d)] group(n=15) and large dose resveratrol [50 mg/(kg·d)] group(n=15).Rats were gavaged with resveratrol or placebo 2 weeks before balloon injury until sacrificed.At 1 and 2 weeks after endothelium denudation,Ⅷ factor immunohistochemical staining and Evans blue staining were used to measure the reendothelialized area.Neointimal formation was determined by HE staining at 2 and 4 weeks after operation.At 1 and 4 weeks after artery injury,endothelial nitric oxide synthase(eNOS) mRNA and protein expression were assayed by reverse transcription-polymerase chain reaction(RT-PCR) and immunohistochemistry,respectively. Endothelial progenitor cells(EPC) were isolated and cultured from rat peripheral blood,which were identified by immunohistochemistry,then the amount of EPC at 1 week after balloon injury were measured by counting DiI-acLDL/FITC-UEA-Ⅰdoublepositive cells in inverted fluorescence microscope. Results 10 mg/(kg·d) resveratrol significantly accelerated reendothelialization at 1 and 2 weeks after balloon injury,50 mg/(kg·d)could not.10 mg/(kg·d) resveratrol markedly inhibited neointimal formation at 2 and 4 weeks after operation,however,50 mg/(kg·d) only reduced neointimal formation at 4 weeks after operation,which was not as effective as previous one.The expressions of eNOS mRNA and protein were potently enhanced in 10 mg/(kg·d) resveratrol group,but not in 50 mg/(kg·d) group.10 mg/(kg·d) resveratrol also significantly increased the amount of EPC in rat peripheral blood at 1 week after operation compared with placebo-treated group(32.46±6.52 vs 21.58±3.69,p<0.05),while the results of 50 mg/kg group did not reach statistical difference(22.48±6.89 vs 21.58±3.69,p<0.05). Conclusions Small dose resveratrol could markedly increase the expression of eNOS,enhance the mobilization of EPC as well as accelerate reendothelialization and reduce neointimal formation compared with placebo-treated group.However,large dose resveratrol only attenuated the intimal hyperplasia at 4 weeks after operation.

Abstract:Aim To investigate whether dehydroepiandrosterone(DHEA) can retard atherosclerosis formation by inhibiting the expression of vascular cell adhesion molecule-1(VCAM-1) and whether all-trans retinoic acid can promote this action. Methods The rabbits were fed with high cholesterol diets for 10 weeks.Then serum lipid levels of all rabbits were measured and the aorta was sampled for morphological observation.Using immunohistochemistry and reverse transcription polymerase chain reaction(RT-PCR),the effect of DHEA on the expression of VCAM-1 protein and mRNA were determined in the aorta of high cholesterol-fed rabbits.In vitro cultured THP-1 monocytes,the expression of VCAM-1 protein and mRNA intervened by DHEA in different density were determined by immunocytochemistry and RT-PCR. Results The thickness of the aortic tunica intima and the aorta atherosclerosis plaque area in the rabbits intervened by DHEA were lowered by 59% and 48% compared with high cholesterol-fed rabbits.The expressions of VCAM-1 protein in the rabbits intervened by DHEA(0.1920±0.0034) were reduced significantly compared with high cholesterol-fed rabbits(0.3846±0.0198).And the expression of VCAM-1 mRNA in the rabbits intervened by DHEA(0.6856±0.0286)were also reduced significantly compared with high cholesterol-fed rabbits(1.0893±0.1089).In vitro cultured THP-1 monocytes,when DHEA in different dose was added into the medium simultaneously,oxidized low density lipoprotein(ox-LDL)-induced VCAM-1 expression was decreased.The expressions of VCAM-1 mRNA in the THP-1 monocytes intervened by DHEA(0.2988±0.0312) were reduced significantly compared with ox-LDL-induced THP-1 monocytes(0.6236±0.0237)when DHEA is 5 μmol/L. After all-trans retinoic acid was added,the change of each index wasn't obvious(p<0.05). Conclusions DHEA showed inhibiting effects on the VCAM-1 expression in both the aorta of high cholesterol-fed rabbits and ox-LDL-induced THP-1 monocytes. That may be one of the mechanisms of antiatherosclerotic action of DHEA. But all-trans retinoic acid have no obvious effect on the VCAM-1 expression in this action.

Abstract:Aim To investigate the effects of Kruppel-like factor 4(KLF4) overexpression on the expression of heat shock protein25(HSP25). Methods Two stable cell lines were made by transforming pcDNA3.1/Myc-His(-) or pcDNA3.1/Myc-His-KLF4 into C₂C₁₂ cell.Reverse transcription polymerase chain reaction(RT-PCR) and Western Blot were employed to study the influence of KLF4 on the expression of HSP25 mRNA and protein respectively under normal physiological and heat shock conditions. Results Under normal physiological condition,the expression of HSP25 mRNA and protein in these two cell lines are relatively low.However,HSP25 mRNA level in KLF4 over expressed cell was significantly higher than that of empty vector cell lines not only under normal conditions but when recovered one hour and three hours after heat shock. Six hours after heat shock,the levels of HSP25 mRNA showed no significant difference between these two cell lines.Under both normal physiological conditions and different time intervals during the recovery of heat shock,the HSP25 protein level was higher in KLF4 over expressed cell line than that in the vector line. Conclusions Under both physiological and heat shock conditions,KLF4 over expression can enhance the expression of HSP25 in the myogenic C₂C₁₂ cell.

Abstract:Aim To investigate the effect of L-Aanginine and aminoguanidine on serum nitric oxide,nitric oxide synthase activity and renal function of diabetic rats. Methods Sixty healthy Wistar rats were involved in the study.The 24 hr urinary protein excretion(UPE),serum levels of nitric oxide(NO), total nitric oxide synthase(NOS) activity,inducible nitric oxide synthase activity and constructive nitric oxide synthase activity were detected to the rats.Streptozotocin(60 mg/kg) was administrated in the rats.The Streptozotocin(STZ) diabetic rats were randomly divided into diabetes control group,L-aanginine group and aminoguanidine group.At the end of 8 weeks after STZ administration,the above five indexes of the rats were detected and statistical analysis was carried out. Results Compared with normal rats: 24hUPE(43.92±7.38 mg),iNOS(19.75±3.85 kU/L) and NO(42.2±6.92 μmol/L) of the rats in diabetes(DM) control group increased significantly(p<0.01,p<0.05).In the rats of L-aanginine group,both 24hUPE(100.47±43.42 mg) and NO(67.34±18.87 μmol/L) increased significantly(p<0.01).In the rats of Aminoguanidine group,24hUPE(22.33±3.47 mg) increased while both tNOS(23.34±3.10 kU/L),iNOS(14.84±1.98 kU/L) and cNOS(8.50±2.25 kU/L) decreased(p<0.01,p<0.05).Compared with the diabetes control group,both 24hUPE and NO increased(p<0.05) in L-aang group at the end of 8 weeks.There was no obvious differences in tNOS,iNOS and cNOS levels in L-aanginine group,and the five indexes were significantly decreased in Aminoguanidine group(p<0.05).Compared with L-aang group,the five indexes were obviously decreased in Aminoguanidine group(p<0.05). Conclusion In early stage of diabetic nephropathy,administration of L-aanginine is harmful to the renal function while aminoguanidine is beneficial to the kidney via increasing or decreasing NO and NOS.

Abstract:Aim To explore the cell apoptosis and inducible nitric oxide synthase(iNOS) expression in the cultured endothelial cells induced by tumor necrosis factor(TNF-α) and angiotensin Ⅱ(AngⅡ). Methods The cultured endothelial cells were treated with TNF-α(10 μg/L) and AngⅡ(1 μmol/L) in absence and presence of pyrroledithiocarbomate(PDTC);the mRNA of iNOS was measured by reverse transcriptionpolymerase chain reaction(RT-PCR),the protein of iNOS and IκBα were assessed by Western blotting,the activity of nuclear factor-κB(NF-κB) was evaluated by electrophoretic mobility shift assay(EMSA),and the cell apoptosis was detected with TUNEL. Ruselts The mRNA and protein of iNOS were significantly increased in the endothelial cells induced by TNF-α and AngⅡ(p<0.05) and PDTC could prevent this increase;at the same time,TNF-α and AngⅡ could increase the apoptosis of cells(p<0.05) and PDTC could prevent this increase. Conclusion TNF-α and AngⅡ induced the up-regulation of iNOS and the cell apoptosis,and the NF-κB play a key role in this process.

Abstract:Aim To investigate the role of the p38 mitogen-activated protein kinase(p38MAPK) on the high glucose-mediated damage to human umbilical vein endothelial cell(hUVEC) and to investigate the effect of the protein kinase C(PKC) dependent pathway on the activation of glucose on p38MAPK. Methods HUVEC were isolated from umbilical cords of normal pregnancies. HUVEC were exposed for 72 h to 5 m(control),22 mmol/L glucose(HG),phorbol myristate acetate(PMA,a PKC agonist),GF109203X(a general PKC-specific inhibitor),SB₂03580(a p38MAPK-specific inhibitor).The expression of phospho-p38MAPK protein and p38MAPK mRNA were detected by Western-blot and reverse transcription polymerase chain reaction(RT-PCR)respectively.The apoptosis of hUVEC were quantitated by flow cytometry using propidium iodid staining. Results Hight glucose and PMA increased the expression of phospho-p38MAPK,p38MAPK mRNA and apoptosis of hUVEC significantly.Incubation of hUVEC with high glucose for 72 h increased the expression of phospho-p38MAPK,p38MAPK mRNA and apoptosis of hUVEC(0.605±0.0407,0.447±0.0252, 16.8%) versus incubation with low glucose(0.189±0.0103,0.313±0.0153,5.15%,p<0.05) respectively.But the expression of phospho-p38MAPK,p38MAPK mRNA and apoptosis of hUVEC were inhibited by GF109203X and SB₂03580. Conclusions The activation of p38MAPK may accelerate the high glucosemediated damage to hUVEC.Hyperglycemia can partly activate p38MAPK by PKC dependent pathway.p38MAPK-specific inhibitor may protect hUVEC in the high glucose-mediated damage.

Abstract:Aim To study the effect of 2,3-dioxoindoline on experimental atherosclerosis in quail and its possible mechanisms. Methods Atherosclerosis model in quail was established and divided randomly as group of 2,3-dioxoindoline(20,60,120 mg/kg),lovastatin(79.5 mg/kg),model and control.The lipid levels in serum were detected at the end of 5th and 8th week respectively.The aorta,myocardium and liver were examined histopathologically and so were the level of total superoxide dismutase(SOD),glutathione peroxidase(GSH-Px) and total antioxidant capacit(T-AOC) while reduced malondiadehyde(MDA) in serum at the end of 8th week. Results At the eighth weekend compared with model group,2,3-dioxoindoline decreased the levels of total cho-lesterol(TC)(p<0.01),triglyceride(TG)(p<0.01),low density lipoprotein cholesterol(LDLC) and apolipoprotein B(p<0.05,p<0.01),increased high density lipoprotein cholesterol(HDLC) and apolipoprotein A in serum.At the same time,TC and TG in the liver,myocardial and aortic wall were reduced(p<0.05,p<0.01),the degree of atherosclerotic lesion in aorta and coronary artery and fatty degeneration of liver in 2,3-dioxoindoline group was reduced(p<0.05,p<0.01),the level of the serum SOD,GSH-Px and T-AOC was increased while MDA level was reduced(p<0.05,p<0.01). Conclusions Beforehand administration of 2,3-dioxoindoline can inhibit atherosclerotic lesion probably due to decreasing blood lipid level and antioxidation.

Abstract:Aim To investigate the effect of atorvastatin on intimal hyperplasia of carotid artery after adventitia removal in spontaneously hypertensive rats (SHR). Methods Thirteen-week-old male SHR(n=24) removed right carotid artery adventitia were randomized into three groups(n=8,each): SHR group,atorvastatin group and valsartan group.8 age-matched male Wistar-Kyoto rats were selected as the normal control group(WKY group).Plasma and carotid artery angiotensinⅡ(AngⅡ) levels were measured by radioimmunoassay.Lumen cross section area(LA),intraelastic layer area(IELA) and extraelastic layer area(EELA) were measured by computed video processing,and the ratio of(IELA-LA)/(EELA-IELA) was calculated.The expression of angiotensin converting enzyme-2(ACE-2) protein was determined by immunohistochemistry method.The expression of ACE-2 mRNA was evaluated by reverse transcription-polymerase chain reaction(RT-PCR). Results Compared with adventitia integrity,the intimal hyperplasia in adventitia removal was exacerbated significantly(p<0.01),and it was markedly inhibited both in atorvastatin and valsartan group(all p<0.01).Carotid artery AngⅡ level in adventitia removal was significantly higher than that in adventitia integrity(p<0.01),while the expression of ACE-2 mRNA and protein in adventitia removal was markedly lower than that in adventitia integrity(p<0.01).Compared with SHR group,carotid artery AngⅡ level in atorvastatin group were reduced significantly(p<0.01),whereas plasma AngⅡ level,the expression of ACE-2 mRNA and protein were increased markedly(all p<0.01). Conclusions Intimal hyperplasia in carotid artery after adventitia removal in SHR is markedly reversed by atorvastatin,which may be related to local ACE-2 up-regulation.

Abstract:Aim To observe the effect of Berberine on the levels of endothelium-1 (ET-1), nitric oxide (NO) platelet derived growth factor (PDGF), transfer growth factor-β1 (TGF-β1) and intima hyperplasia and vascular remodeling after balloon withdrawal injury of rabbit carotid artery, and to evaluate its mechanism. Methods Fourty Japanese rabbits were allocated randomly into 4 groups: artificial group( n = 7), model group( n = 11), berberine group ( n = 11) and simvastatin group( n = 11). The balloon endothelium denud-ation were made in carotid artery of all rabbits of the later three groups in the condition of anesthesia, and they were injected respectively with 0.9% sodium chloride, berberine and simvastatin liquid (2.5 mg/kg everyday) . After 15 days, the levels of ET- 1, NO and PDGF, TGF-β1 of all groups were detected; at the same time, we observed the morphologic change of injured artery and took photos, and intimal thickness (IT), intimal area(IA), luminal area (LA), internal elastic lamina (IEL), medial area (MA) and external elastic lamina (EEL) of all groups were measured with the system of computer photo analysis, IA/MA and intima hyperplasia index(IHI)were computed. Results The concentration of NO of berberine group (65 ±13) were increased significantly compared with model group (32 ± 13) and simvastatin group (40 ± 16) ( P < 0. 01); the levels of ET - 1 and PDGF, TGF-β1 of berberine group( 58 ± 11,145 ± 12,163 ± 33) were markedly decreased compared with model group (91 ± 16,183 ±33,210 ±28) (p<0.01). IT, IA, IA/MA and IHI of berberine group(32.91±4.20,10.22 ± 1.91,0.31 ±0.06,19.51± 3.48) were decreased significantly than model group (59.54± 7.17,18.66 ± 4.57, 0.62±0. 14, 28.32±4.25)but higher than artificial group(14.11 ± 2.95,2.73 ± 0.35,0.10 ± 0.03, 9.22 ± 0.87) ( P < 0.01); and LA, IEL, EEL of berberine group (48.56±4.71, 59.45±2.42, 91.12 ±7.19) were increased deadly than model group (27. 33 ±3.47, 45.82±4.65, 75.75±1.05) and artificial group(35.08 ± 8.00, 37.14±3.25, 68.38 ± 3.30) (P < 0.01), but MA of 4 groups have no marketable change ( P > 0.05). Conclusion Berberine can increase the levels of NO, decrease the concentration of ET-1, PDGF, TGF-β1; and make LA, IEL, EEL enlarged but IT, IA, IA/MA, IHI reduced; which can be the possible mechanism that inhibits intima hyperplasia and vascular remodeling.

Abstract:Aim To observe the expression of brain-derived neurotrophic factor (BDNF) and Semaphorin 3A(Sema 3A) after focal cerebral ischemia,and to study the neuroprotective effects of puerarin. Methods The model of focal cerebral ischemia was established by occluding middle cerebral artery(MCAO).Dynamic changes of BDNF and Sema 3A positive neurons at different time were observed with method of immunohistochemistry. Results The number of BDNF positive neurons increased after 6 h of ischemia,and reached its peak at the time of 1 d after ischemia.Compared with treatment group and ischemic group,the levels of BDNF were higher(p<0.05);the number of Sema 3A positive neurons increased after 6 h of ischemia,and reached its peak at the time of 1 d after ischemia,then become normal after 3 d.Compared with treatment group and ischemic group,the levels of Sema 3A were lower(p<0.05). Conclusions After the attack of cerebral ischemia, the expression of BDNF and Sema 3A may be related to the mechanism of neuronic injury and repairment.Puerarin may have protective effects on ischemic neurons.

Abstract:Aim To study the protective effect of fructose-1,6-diphosphate(FDP) on adriamycin(ADR)-induced myocardial damage. Methods 30 SD rats were divided into three groups randomly: control group,ADR group and ADR+FDP group.The changes of heart rate and dry and wet ratio of pulmonary and liver were observed,and the level of creative kinase isoenzyme MB(CK-MB) were measured.The active level of CuZn SOD was examined and its protein level was measured by immunohistochemistry,its gene level expression was measured by half-quantitatire polymerase chain reaction. Result Compared with ADR group,the heart rate change of ADR+FDP group was decreased(p<0.05),the dry and wet ratio was increased(p<0.05),and CK-MB was decreased(p<0.01) obviously.The active level of Cn-Zn SOD was up(p<0.05),the gene and protein expression of Cu-Zn SOD was down(p<0.05). Conclusion FDP has a protective effect on adriamycin-induced myocardial damage.Its mechanism is possibly related with inhibiting oxidation.

Abstract:Aim To study the intracellular apoprotein(a) and apoprotein B₁₀₀ levels of three categories of leukocytes in coronary heart disease,and evaluate the effect of intracellular apoproteins on coronary atherosclerosis status. Methods Patients with no coronary stenosis(n=18)and three-vessel coronary artery disease(n=13)validated by angiography were enrolled in this study.Intracellular apoprotein(a) and apoprotein B₁₀₀ concentrations were measured in monocytes,lymphocytes and granulocytes by flow cytometry. Results It was demonstrated that genes of apoprotein(a) and apoprotein B₁₀₀ would not transcript in leukocytes by reverse transcription-polymerase chain reaction(RT-PCR).But apoprotein(a) and apoprotein B₁₀₀ were expressed in all three categories of leukocytes validated by confocal microscopy and flow cytometry.Stenosis patients had a higher levels of intracellular apoprotein B₁₀₀,represented by mean fluorescence intensity(MFI) in monocytes (189±77 vs 41±13,increased 364%,p<0.01), lymphocytes(102±65 vs 16±6,increased 532%,p<0.01) and granulocytes(417±250 vs 183± 88,increased 128%,p<0.05) than no stenosis patients.And the positive percentage of cells containing apoprotein(a) in lymphocytes,monocytes and granulocytes as well as containing apoprotein B₁₀₀ in granulocytes increased in stenosis patients too. Conclusions All categories of leukocytes can carry apoprotein(a) and apoprotein B₁₀₀,and the intracellular concentrations of apoprotein B₁₀₀ had a close correlation with coronary stenosis.

Abstract:Aim To study the changes of secretory type Ⅱphospholipase A2(sPLA2) in coronary heart disease(CHD) and the relationship with high sensitive Creactive protein(hs-CRP). Methods According to clinical syndrome and angiography,110 patients were enrolled as acute coronary syndrome(ACS) group,63 patients as stable coronary heart(SCHD) disease(SCHD) group and 89 non-CHD patients as control group.Serum levels of sPLA2 was measured by enzyme linked immunosorbent assay(ELISA) in all subjects and the relationship with hs-CRP was studied. Results Compared with control group,the level of serum sPLA2 was higher in CHD group(55.18±11.75 ku/L vs 68.15±16.70 ku/L,p<0.01),which was also higher in ACS group than that in SCHD group(71.32±18.07 ku/L vs 62.63±11.92 ku/L,p<0.01).The level of serum sPLA2 was positively correlated with hs-CRP. Conclusion The increasing level of serum sPLA2 is correlated with CHD and the stability of coronary plaque.sPLA2 may be one of the important inflammation indicators in patients with coronary artery disease.

Abstract:Aim To investigate the relationship between serum concentration of basic fibroblast growth factor(bFGF) and coronary collateral circulation(CCC) and the severity of atherosclerosis. Methods 80 patients with severe coronary stenosis were recruited.The CCC were rated by Rentrop rating system: rate 0(n=26),rate 1(n=22),rate 2(n=18),rate 3(n=14).Serum concentrations of bFGF were measured by ELISA,and the severity of coronary artery atherosclerosis was evaluated by Gensini's score system. Results The serum concentrations of bFGF were 20.75±6.89 ng/L,22.04±5.18 ng/L,27.32±6.14 ng/L and 32.27±12.04 ng/L in patients with CCC rate 0,1,2 and 3 group respectively.The serum concentrations of bFGF was increased with CCC rating(p<0.05).Spearman corelation analysis demonstrated that there was a positive correlation between CCC rating and the serum bFGF concentrations(p<0.01). Conclusions In patients with severe coronary artery disease,serum concertrations of bFGF in groups with better CCC formation were significantly higher than those in groups with bad CCC formation.Serum bFGF concentrations showed a positive correlation with the rating of coronary collateral circulation formation.

Abstract:Aim To evaluate the clinic significance of antibodies to oxidized low density lipoprotein(ox-LDL) in the patients of coronary artery disease(CHD). Method The target population was divided into four groups by his clinic syndrome: stable angina pectoris(SAP);unstable angina pectoris(UAP);acute myocardium infarction(AMI);normal control group(CON).Antibodies to ox-LDL in serum of the patients was measured by enzyme linked immunosorbent assay(ELISA).The stenosis degree of coronary artery was quantitative assayed by Gemini marker. Results The titre of antibodies to ox-LDL in the patients of CHD was obviously higher,especially in the ACS,than that in CON.The titre increased in hysteretic mode,which was highest 7～10 days after hospitalization and was most obviously different between groups.There was no statistical dependence between the titer of antibodies and the stenosis degree of coronary artery. Conclusions There is a positive correlation between the titer of antibodies to ox-LDL and the clinical manifestation of CHD,which reveals that autoimmunity may play an important role in the origin,progress of atherosclerosis(As).And the titer of antibodies to ox-LDL is hoped to be an important marker to evaluate the risk of As.

Abstract:Aim To evaluate the relationship between blood pressure and the range and severity of coronary artery stenosis. Methods 540 inpatients who had been diagnosed with suspicious coronary heart disease(CHD) were carried through coronary angiography.Blood pressure and blood lipoprotein of all patients were measured.Their history of high blood pressure,smoking and diabetes was investigated.All patients were carried with angiography by Judkins way.Based on coronary artery lesion 540 inpatients were separated into two groups: lesion group and no lesion group;based on coronary artery lesion range 540 inpatients were separated into three groups: single vessel disease group,double vessel disease group and triple vessel group. Results Coronary angiography shows that patients in lesion group have more hypertension history(5.85 ±8.87 years),higher level of systolic blood pressure(133±29 mm Hg),diastolic blood pressure(83±13 mm Hg),pulse pressure(51±17 mm Hg) and mean blood pressure(100±14 mm Hg) than that in no lesion groups(1.78±4.27 years,125±21 mm Hg,80±13 mm Hg,48±15 mm Hg and 97±15 mm Hg). There were more hypertension history,higher level of systolic pressure and pulse pressure in single vessel disease group and triple vessel group(7.42±10.10 years,137±21 mm Hg and 54±17 mm Hg) than that in single vessel disease group(4.51±7.21 years,132±19 mm Hg and 49±16 mm Hg),and double vessel disease group(5.76±8.79 years,134±23 mm Hg and 52±17 mm Hg).Difference among three groups had noticeable significance(p<0.05).Severity of coronary artery stenosis was developed with more hypertension history,higher level of systolic blood pressure,pulse pressure and mean blood pressure.Hypertension(OR=0.139,p<0.05),and ages(OR=1.045,p<0.05) were independent risk factors for happening of coronary artery disease by multiple factor regression analysis. Conclusions Opportunity of coronary artery disease was increased with ages and hypertension history.Moreover,higher level of systolic blood pressure and pulse pressure were more harmful than others.

Abstract:Aim To evaluate the relationship between G894T polymorphism(Glu298Asp) in the endothelial nitric oxide synthase(eNOS) gene and coronary heart disease(CHD) in population from various countries. Methods Odds ratios(OR) of genotype frequencies in CHD group against control group were analyzed.All the relevant studies were identified,those unqualified studies were excluded and the publication bias was evaluated.The Meta-analysis software(REVMAN4.2) was applied for investigating the heterogeneity among individual studies and for summarizing all the studies. Results Finally 12 studies entered the present study,including 5 891 cases and 3 392 controls.There was significant difference among individual studies(χ2=63.40,p<0.00001),so the random effect model was used to summarize all the studies.The pooled TT/(GT+GG) OR was 1.52,95% CI was 1.02～2.25(P=0.04). Conclusion The TT genotype of G894T polymorphism in eNOS gene is at moderately increased risk of CHD and may be one of the genetic risk factors of CHD.

Abstract:Aim To explore the relationship of arterial stiffness index(ASI) with carotid artery intima-media thickness(IMT) in hypertensive patients. Methods 124 hypertensive patients who underwent the IMT of carotid arteries were evaluated.They were classified as IMT increased group or no IMT increased group.ASI was measured with YF-1XGYD device.The record of medical history,blood pressure were performed.The biochemical parameters such as blood lipids,glucose and so on were tested. Results There were no significant differences in clinical manifestations between patients of the IMT increased group and no IMT increased group(p<0.05).The ASI value of the IMT increased group was significantly higher than that of the no IMT increased group(p<0.01). Conclusion ASI could be used as an indicator of cardiovascular risk in hypertensive patients.