Abstract:AimTo investigate the effects of hydrogen sulfide(H₂S) on ox-LDL uptake of THP-1-derived macrophages and its underlying mechanisms. Methods Fluorescence microscopy, RT-PCR and western blot were performed. ResultsIncubation of macrophages with DiI-ox-LDL led to ox-LDL uptake of macrophages.Sodium hydrosulfide(NaHS, an H₂S donor) decreased ox-LDL uptake. While DL-propargylglgycine (PPG) exerted opposite effects.Furthermore, ox-LDL markedly induced CD36 mRNA and protein expression in macrophages, which was abolished by NaHS (50 to 100 μmol/L), but enhanced by PPG. Conclusions H₂S inhibits ox-LDL uptake of THP-1-derived macrophages and down-regulates CD36 mRNA and protein expression.

Abstract:AimTo investigate the beneficial effects of nonpeptide angiotensin-(1-7)［Ang-(1-7)］ analogue AVE0991 on ventricular remodeling and cardiac dysfunction in rats induced by myocardial infarction (MI). Methods Forty male Sprague-Dawley rats were randomly divided into sham operation group, control group, AVE0991 group and AVE0991 + A-779 group. MI was induced by left coronary artery ligation. After 4 weeks of treatment, transthoracic echocardiography (TTE) was used to evaluate cardiac function. The left ventricle wet weight was recorded, normalized for body weight. Left ventricle serial sections were dyed with Masson or hematoxylin-eosin (HE) stain to quantify the infarct size and diameter measurement of cardiomyocytes. ResultsFour weeks after MI, rats with MI demonstrated significantly increase in the left ventricular end-diastolic (LVDd) and end-systolic dimension (LVDs) and decrease in interventricular septum end-systolic (IVSs) and end-diastolic thickness (IVSd), left ventricular fractional shorting (LVFS) and left ventricular ejection fraction (LVEF). AVE0991 treatment attenuated the decrease in LVFS (25.5 % ± 7.3 % vs 18.4 % ± 3.3 %, p<0.05) and LVEF (44.8% ± 7.6% vs 32.7% ± 6.5 %, p<0.05) compared to control group. AVE0991 also reduced MI-induced hypertrophy as quantified by myocyte diameter measurements (vs control group, 17.6± 2.4 μm vs 22.9± 3.9 μm, p< 0.05). In addition, left ventricular mass index (LVMI) (2.54 ± 0.25 vs 2.93 ± 0.34, p<0.01) and infarct size (42.6 % ± 3.6 % vs 50.9 % ± 4.4 %, p<0.01) were slightly reduced in AVE0991 group compared to control group. In addition, the specific antagonist for Ang-(1-7), ［D-Ala7］-Ang-(1-7) (A-779), showed a tendency to diminish the protective effects of AVE0991. ConclusionAVE0991 could attenuate ventricular remodeling and improve cardiac function induced by acute myocardial infarction in rats, its effects may play a role through the specific Mas receptor for Ang-(1-7).

Abstract:Aim To investigate the protective effects of Jiawei Buyang Huanwu decoction on vascular stenosis and on the nitric oxide(NO) system after iliac artery were injured by balloon in diet-induced atherosclerotic rabbits. Methods 24 male New Zealand albino rabbits were equally randomized into control group, model group and drug group. The iliac arteries of the rabbits in the latter two groups were subjected to balloon injury. Four weeks later, serum NO synthases (NOS) activity and endothelial nitric oxide synthase (eNOS) level was assayed, endothelial hyperplasia, eNOS protein and mRNA expression were observed in injured iliac artery. Results Optical microscope revealed narrowed vascular lumen, thicken intima and numerous arteriosclerotic plaques in the model group compared with the control group, whereas the vascular lumen and intima thickness remained basically normal in drug group.The serum NO level and total NOS activity were higher in drug group than that of model group.Immunohistochemistry and RT-PCR results showed that eNOS protein and mRNA expression was stronger in rabbit iliac artery of drug group than that in model group.Conclusion Jiawei Buyang Huanwu decoction can lessen intimal hyperplasia and vascular stenosis in iliac artery injury rabbits, and this effect is possibly related with that Jiawei Buyang Huanwu decoction activated the NO system.

Abstract:AimTo investigate the effect of ODN1826, a TLR9 ligand, on perilipin 2 expression in macrophages. Methods Real-time PCR and Western blotting were performed to detect perilipin 2 expression.Transient transfection and luciferase assay were employed to measure the perilipin 2 promoter activity. ResultsODN1826 significantly induced perilipin 2 expression in a dose and time dependent manner in macrophages.ODN1826 markedly enhanced perilipin 2 promoter activity, and this process requires Ets/AP-1 activity. Conclusions TLR9 signal pathway stimulated perilipin 2 expression in macrophages, in addition, ODN1826-induced perilipin 2 promoter activity requires Ets/AP-1 activity.

Abstract:AimTo investigate the effect of C-reactive protein (CRP)on rat bone marrow-derived endothelial progenitor cells (EPC)involved into vasculogenesis and functional activity in vitro, and discuss possible mechanism of CRP during progression of atherosclerosis.MethodsEPC were separated from bone marrow of rat with density gradient centrifugation, and characterized as DiI-ac-LDL/FITC-UEA-l double positive cells detected by laser confocal microscopy.EPC were cultured with CRP of different concentrations (0， 1, 5 and 10 mg/L) for 24 h.A co-culture model of EPC and rat cardiac microvascular endothelial cells (CMEC) was used to analyze the effect of CRP on EPC involved into lumen formation in vitro.Proliferation viability, migration, vasculogenesis, and protein expression of EPC were assayed by MTT, Transwell chamber, Matrigel, Western blotting respectively.ResultsCRP dose-dependently reduced the number of EPC involved into capillary-like structures of CMEC, weakened proliferation viability of EPC, reduced the number of migration and lumen formation, up-regulated the expression of Bax protein, and down-regulated the expression of Bcl-2 protein, integrin β2, endogenous vescular endothelial growth factor (VEGF).ConclusionCRP may impair EPC-mediated neovascularization by weakening its functions, which leads to progression of atherosclerosis.

Abstract:AimTo investigate the therapeutic effect of Hydrogen inhalation on cardioplumonary bypass(CPB) induced acute lung injury(ALI) in Beagle dogs.MethodsCPB models were set up with living Beagle dogs.20 dogs were divided into hydrogen inhalation group(H₂ group) and control group(C group) randomly.Pulmonary artery pressue(PAP),pulmonary capillary wedge pressure(PCWP) and pulmonary vascular resisitance(PVR) were recorded at the five defined time points, artery blood samples were obtained for blood gas analysis and determined plasma cytokine levels(TNF-α,IL-6,IL-8) at the mean time.At the end of the research lung tissue were acquired for evaluation of pulmonary malondiadehyde(MDA)， superoxide dismutase(SOD), myeloperoxidase(MPO)，the ratio of wet to dry lung weight(W/D) and lung histopathology.Neutrophils and total protein content in bronchoalveolar lavage fluid(BALF) were also determined.ResultsCompared with control group, PAP,PCWP and PVR were significiantly improved in H₂ group.Neutrophils,total protein,differentiation in the lung W/D and cytokine content were lower than those in control group.Pulmonary MDA and MPO in hydrogen group were lower than those in control group, and the SOD was higher than that in control group.Histologic analysis showed that less lung injury by microscope examination was seen in hydrogen group than that in control group.Conclusion2% Hydrogen inhalation can alleviate CPB induced lung by inhibition of inflammatory and oxidative stress.

Abstract:AimTo investigate the effect and mechanism of prostaglandin E1 on atherosclerotic vulnerable plaque in rabbits.Methods22 rabbits were fed a 1% cholesterol diet 2 weeks prior to and 7 weeks after balloon injury of the abdominal aorta. Thereafter the atherogenic diet was replaced with a regular diet, and rabbits were randomly divided into 3 groups for 4 weeks treatment: control group, prostaglandin E1 group and simvastatin group. At the end of week 13, all rabbits were challenged with injection of Chinese Russells viper venom and histamine. Serum, plaque morphology, plaue composition and inflamatory expression studies were performed.ResultsProstaglandin E1 did not alter serum lipid levels. Prostaglandin E1 significantly increased the thickness of the fibrous caps (101.72±34.89 μm vs 79.86±16.98 μm, p<0.01) and decreased plaque vulnerability index (0.94±0.27 vs 3.83±1.45, p<0.01); Prostaglandin E1 attenuated macrophage accumulation (p<0.01) and MMP-1, MMP-9 expression (both p<0.01) within the plaque, and there was no statistical difference between prostaglandin E1 group and simvastatin group.ConclusionProstaglandin E1 effectively enhanced stability of vulnerable plaque in rabbit model independent of serum lipid levels, in which inhibiting macrophage accumulation and inflammatory expression within plaque may play an important role.

Abstract:AimTo observe the effect of fluvastatin on the expression of matrix metalloproteinase-1(MMP-1), tissue inhibitors of matrix metalloproteinase-1(TIMP-1), and intracellular adhesion molecule-1(ICAM-1) induced by visfatin in cultured human umbilical vein endothelial cells（HUVEC）, and to explore the effect and mechanism of anti-inflammatory of fluvastatin.MethodsHUVEC were cultured in vitro, the HUVEC were pretreated with fluvastatin at different concentrations (10-7 mol/L,10-6 mol/L,10-5 mol/L) for 20 minutes before incubated with the visfatin of 800 μg/L for 24 hours.The cellular total RNA were extracted by TRNzol reagent.The expression of MMP-1, TIMP-1 and ICAM-1 mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR).The results of gel electrophoresis were analyzed with a computer scanning system.ResultsDifferent concentrations of fluvastatin could inhibit the expression of MMP-1 mRNA and ICAM-1 mRNA induced by visfatin in a dose-dependent manner.Different concentrations of fluvastatin could up-regulate the expression of TIMP-1 mRNA induced by visfatin.ConclusionFluvastatin could inhibit inflammatory response in vascular endothelial cells induced by visfatin in a dose-dependent manner, which could protect endothelial cells against the functional disorder, and prevent the development of atherosclerosis.

Abstract:AimTo observe the expression of interleukin-10 (IL-10) on cerebral vascular endothelial cells in smoking rats, and to discuss the mechanism of ischemia in brain caused by smoking.Methods 60 health Wistar rats were divied into 6 groups: normal control group, sham exposure group, exposed cigarette smoke 30 days group, exposed cigarette smoke 30 days then stopping exposion for 30 days group, exposed cigarette smoke 90 days high dose group and exposed cigarette smoke 90 days low dose group. The expression of IL-10 were observed in smoking rats by immunohistochemistry stain.Results The expression of IL-10 in normal control group and sham exposure group were more. The expression of IL-10 in exposed cigarette smoke 90 days high dose group were significantly lower than those in the other passive smoking groups. The expression of IL-10 in exposed cigarette smoke 30 days then stopping exposure for 30 days group were significantly higher than those in the other passive smoking groups. The expression of IL-10 in the passive smoking groups were significantly lower than those in control group and the sham exposure group (p<0.05).ConclusionsSmoking can decrease IL-10 expression in endothelial cell, which plays an important role in ischemic cerebral vascular disease.

Abstract:AimTo investigate the effect of percutaneous transluminal renal arterioplasty (PTRA) on blood pressure and renal function in patients with renal artery stenosis (RAS).Methods 23 patients with renal artery stenosis treated by PTRA were selected as the study subjects and their clinical data were retrospectively analyzed to observe the changes in blood pressure and renal function and to analyze the efficacy.Results23 patients were successfully implanted the renal artery stent with no serious intraoperative and postoperative complications, the residual stenosis were less than 30%and the surgical successful rate was 100%. Patients were followed up for 12 months, 3 cases were cured of hypertension, 17 cases improved, the total improvement rate was 86.9%; 6 cases were improved of renal function, 13 cases of stability, the total benefit rate was 82.6%. Systolic blood pressure (SBP) reduced from 180.3±35.6 mmHg to 131.2±25.4 mmHg, diastolic blood pressure (DBP) reduced from 106.2±21.5 mmHg to 80.6±14.2 mmHg, serum creatinine reduced from 286.4±113.7 μmol/L to 166.5±84.8 μmol/L, the difference between before and after surgery was significant (p＜0.05).ConclusionsPTRA and renal artery stenting for the treatment of RAS has high success rate. It can control the blood pressure and stabilize the renal function, while its long-term efficacy needs further investigation.

Abstract:AimPulse wave velocity (PWV) reflects arterial stiffness and may provide an integrated index of vascular status and cardiovascular disease (CVD) risk. Individual components of the metabolic syndrome(MS) are well-established cardiovascular risk factors.Thus we conducted a cross-sectional study in continuous ambulatory peritoneal dialysis (CAPD) patients to explore the association of MS components with PWV. MethodsPrevalent 148 CAPD patients, were categorized according to the number of traits of the MS into one of three groups (No MS, Risk of MS, MS). Aortic stiffness was assessed by carotid-femoral PWV (C-F PWV). Results C-F PWV was positively associated with age(r=0.427, p<0.01), systolic blood pressure (r=0.444, p<0.01), pulse pressure (r= 0.498, p<0.01), and serum glucose (r=0.366, p<0.01).C-F PWV was negatively associated with serum albumin(r =－0.216, p<0.05).In a multivariate regression analysis, PWV was independently determined by age (p<0.01) and MS score (p=0.01). Adjusted R² of the model was 0.24. ConclusionMS traits were closely associated with an increased C-F PWV, even after adjustment for confounders. This suggests that commonly recognized MS criteria are also useful when predicting CVD in CAPD patients.

Abstract:AimTo investigate the plasma levels of periostin protein and vascular endothelial growth factor (VEGF) in the patients with coronary heart disease (CHD), and to analyse the relationship and clinical significance between periostin protein and VEGF.Methods Plasma levels of periostin protein and VEGF in CHD patients (n=180) and healthy controls (n=52) were measured by enzyme-linked immunosorbent assay (ELISA). The patients with CHD were divided into four gropus: acute myocardial infarction (AMI)group (n=58), old myocardial infarction (OMI) group (n=30), unstable angina pectoris (UAP) group (n=40) and stable angina pectoris (SAP) group (n=52).ResultsThe plasma levels of periostin were not only significantly higher in CHD patients compared to healthy controls in the order of AMI group>UAP group>OMI group>SAP group> healthy controls, but also had statistical significance except OMI group vs SAP group and UAP group vs OMI group (p<0.05 or p<0.01). The plasma levels of VEGF were significantly higher in CHD patients compared to healthy controls in the order of AMI group>UAP group>OMI group>SAP group> healthy controls ( p<0.05 or p<0.01 ). The plasma levels of periostin was positively correlated with VEGF (r=0.593，p<0.01).ConclusionsThe plasma levels of periostin significantly correlated with CHD. The increase in plasma levels of periostin may be one of the pathogenesis of coronary heart disease, and periostin may promote

Abstract:AimTo investigate the prevalence of aortic valve sclerosis (AVS) in the high-risk group of cardio-cerebral vascular events, and to evaluate the clinical risk factors of AVS.Methods1058 individuals were enrolled in the cohort of the community of the Capital Steel Corporation in 2005.Participants were excluded if they had a history of any of the following diseases: rheumatic valve disease, bicuspid aortic valve malformation, prosthetic valve replacement, aortic valve stenosis.Risk factor status (including smoking， hypertension and diabetes etc) were adjudicated based on a review of data collected from hospitalizations and outpatient records.Total cholesterol and high density lipoprotein (HDL) cholesterol, triglycerides were measured from blood samples.Transthoracic echocardiography was performed to access the aortic valve sclerosis.And according to the results of the echocardiography, population was divided into two groups: AVS group and non-AVS group.Results1039 individuals were included in this study finally with mean age 62.47±8.99 years old.The prevalence of hypertension of 1039 individuals was 68.72% and of diabetes mellitus was 25.89%.AVS was present in 401 individuals (38.59%).The risk factors of AVS included age (OR=1.589,p<0.001), male(OR=2.263,p<0.001）, hypertension(OR=1.296,p=0.063）, diabetes mellitus (OR=1.794，p<0.001）.However after multivariate Logistic regression analysis, the independent risk factors of AVS included age (OR=1.507,p<0.001), male(OR=1.974,p=0.003), hypertension(OR=1.428,p=0.015), diabetes mellitus (OR=1.719,p<0.001）.ConclusionMultiple risk factors may involve in the progress of AVS.AVS and arteriosclerosis have some same risk factors which indicates that some factors for atherosclerosis may also play an important role in the prevalence of aortic valve sclerosis.

Abstract:AimTo investigate whether atherosclerosis may be accelerated by lipoprotein-associated phospholipaseA₂(Lp-PLA₂) in patients with chronic renal failure(CRF). Methods 100 patients of CRF and 40 healthy volunteers were involved in the study.The levels of plasma Lp-PLA₂ were determined by enzyme-linked immunosorbent assay (ELISA).Intima-middle thickness (IMT) and prevalence atherosclerotic plaques of the extrcranial common carotid artery were measured by high-resolution B-mode ultrasonography. The CRF group level of plasma Lp-PLA₂ was compared with the control group.The levels of plasma Lp-PLA₂ were compared between the different groups in patients with CRF.The multiple stepwise regression analysis was used for the multi-factor of affecting the carotid artery IMT. ResultsHigher plasma Lp-PLA₂ levels were found in patients with CRF(232.16±59.36　μg/L） as compared with those in healthy controls(129.47±29.72　μg/L,p<0.01）. Lp-PLA₂ levels in dialysis patients(261.84±50.82　μg/L） were significantly higher than in pre-dialysis patients(204.73±53.95　μg/L,p＜0.01）. Lp-PLA₂ levels increased with the progression of renal dysfunction and inversely correlated with creatinine clearance(Ccr)(r＝－0.567,　p<0.01).Patients with carotid artery atherosclerotic plaques showed significantly higher levels of Lp-PLA₂(281.33±39.72 μg/L） as compared with patients without carotid artery atherosclerotic plaques(188.46±35.02 μg/L,p<0.01). By multiple stepwise regression analysis strong association was still present between Lp-PLA₂ levels and carotid artery IMT(β＝0.735,p<0.01) in the CRF patients. 　ConclusionThe results indicate that atherosclerosis is associated with increase of plasma Lp-in CRF patients.The elevated levels of Lp-PLA₂ may be involved in the occurrence and development of atherosclerosis for CRF patients.

Abstract:AimTo research on the influence of variety of cardiovascular disease on carotid artery intima-media thickness（IMT）and heart rate variability（HRV） in elderly hypertension patient.Methods192 senile hypertension were selected for A group,152 senile hypertension with coronary heart disease (CHD) as B group, 145 senile hypertension with diabetes(DM) as C group,184 senile hypertension with CHD and DM as D group.Clinical features, carotid atherosclerosis and Holter report (supervision) of four groups were analyzed.ResultsFasting blood-glucose (FBG), serum total cholesterol (TC), and IMT in patients of D group were significantly different from those in A,B,C group (p<0.05).The average heart rate and night heart rate were highest in D group.The incidence of ventricular premature beat, atrial arrhythmia, ischemic ST segment depression and HRV in the Holter reports of patients in D group was higher than A, B, C group(p<0.05).ConclusionFBG and TC are highest in senile hypertension with CHD and DM.The incidence of atherosclerotic plaque significantly increases in senile hypertension with CHD and DM.And also it tends to showing up depression HRV obviously.

Abstract:AimTo investigate the association of P-selectin gene single nucleotide polymorphisms (SNP) and susceptibility to acute myocardial infarction (AMI) in a Chinese population, and to analyze association of serum levels and genotypes of P-selectin with AMI.Methods P-selectin gene －2123 G/C single nucleotide polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing among 150 AMI patients and 160 age and sex matched controls in a Chinese population, and serum level of P-selectin was determined by enzyme-linked immunosorbent assay (ELISA).ResultsSerum levels of P-selectin in AMI patients were significantly higher than those of controls (p<0.05), the distributions of P-selectin gene －2123 G/C polymorphism were significantly different between AMI group and control group (p<0.05). The relative risk suffered from AMI of －2123 C allele was 1.625 times of the G allele carriers (OR=1.625, 95%CI was 1.177～2.244, p=0.003); the serum levels of P-selectin C allele carriers was significantly higher than no carriers (p<0.05).ConclusionsP-selectin gene －2123 G/C polymorphism was associated with AMI, －2123 C allele is an important genetic susceptibility gene for AMI. In which the P-selectin C allele carriers may increase risk by enhancing the P-selectin expression in the pathogenesis of AMI.

Abstract:Vascular endothelial cell injury or dysfunction has been implicated in the onset and progression of cardiovascular diseases including atherosclerosis. Numerous studies have indicated that endothelial cells oxidative and inflammation play an important role in initiation and progress of atherosclerosis. More and more studies have demonstrated that interleukin-4 can increase oxidative stress by inflammatory mediators such as cytokines, chemokines and endothelial cell adhesion molecule. Interleukin-4 can accelerate apoptosis and promote endothelial cell updates through a variety of signaling pathway, which can lead to vascular endothelial dysfunction. These studies will most likely provide new targets or direction for the prevention and treatment of vascular inflammatory diseases such as atherosclerosis.

Abstract:Endothelial microparticles are submicron membrane vesicles shed from plasma membranes in response to endothelial cell activation or injury and play a major biological role in adhesion, inflammation and angiogenesis.Recent studies indicate that endothelial microparticles are involved in the development of coronary heart disease for their close association with oxidative stress, endothelial dysfunction and vulnerable plaque rupture.Thus, elucidating their role and their mechanisms of formation will bring new insights into the understanding of coronary heart disease.

Abstract:Cystatin C concentration is very stable because of its independence of factors such as age, sex, and body composition，which has been extensively studied as an endogenous serum marker of glomerular filtration rate. However, recent studies indicated that Cystatin C concentration had correlation with cardiovascular events.Cystatin C may participate in the pathogenesis of cardiovascular disease such as atherosclerosis and aneurism.