Abstract:Aim To explore the effect of enhanced external counterpulsation (EECP) against atherosclerosis and its endothelial mechanisms. Methods Twelve hypercholesterolemic pigs were randomly divided into the hyperlipidemia and EECP groups. After EECP,amount to 36 hours,the coronary arteries and abdominal aortas were sampled for histopathologic and ultrastructural examination. The endothelial cells (EC) were collected from thoracic aorta for proteomic study. Results Compared with the hypercholesterolemic animal receiving EECP,much more plaques were found in the hypercholesterolemic animal without EECP. The plaque/intimal area ratio of the aorta decreased significantly in animals receiving EECP (1.27%±0.35%) versus (7.83%±2.39%) in those without EECP,P<0.05. Lipid deposition,endothelial damage and proliferation of smooth muscle cells were less severe in animals receiving EECP than those without EECP. Moreover,eight kinds of proteins were higher expressed in ECs from animals receiving EECP than from those without EECP. Conclusion EECP could prevent atherosclerotic lesion progress by repairing damaged endothelia caused by hypercholesterolemia.

Abstract:Aim To study the effect of thalidomide on the atherosclerotic lesions induced by abnormal shear stress in the carotid arteries of New Zealand Rabbits. Methods After assembled silastic collars (length 8 mm,intra-diameter 1.4 mm) around the right carotid arteries of all the New Zealand White rabbits,they were randomly divided into three groups:control group (chew diet,n=13),high-fat group (with 2% cholesterol,n=13) and high-fat added with thalidomide (20 mg/kg) group. The rabbits were fed for 9 weeks. Serum was collected at the first week and the end week. Plasma triglyceride (TG),total cholesterol (TC),high density lipoprotein (HDL),and low density lipoprotein (LDL) were determined by commercially enzymatic methods. the atherosclerotic lesions in carotid arteries were determined by using Sudan Ⅳ staining and HE staining. Results There was no obvious difference in body weight between three groups before and after experiment. Plasma TG,TC,LDL and HDL concentrations were markedly increased in high-fat group and high-fat added with thalidomide group compared with Control (P<0.05). Compared with high-fat group,the content of TC,LDL,HDL and TG in high-fat added with thalidomide group had not statistical difference. Plaques were identified to exist in the upstream from the cast obviously more than downstream from the cast in sizes in high-fat group with Sudan Ⅳ staining. The atherosclerotic lesions in high-fat added with thalidomide group existed in the upstream mainly,and the sizes were less than that in high-fat group. Compared with no atherosclerotic lesion in the cast,there were lipid accumulation and cells infiltration in atherosclerotic lesions in high-fat group with HE staining,which extended to the lumina. The atherosclerotic lesions in the downstream existed with neointima formation. The main lesion in high-fat added with thalidomide group was neointima formation in the upstream,and no obvious lesion in downstream and the cast. There were no lesions the carotid arteries in the control group. Conclusion Abnormal shear stress may induce the atherosclerotic lesion formation in the carotid arteries in New Zealand Rabbits,and which could be inhibited by thalidomide.

Abstract:Aim To study the effects of NAD(P)H oxidase subunits p22phox on endothelial reactive oxygen species (ROS) induction and cell apoptosis induced by high-glucose. Methods Human umbilical vein endothelial cell (hUVEC) were divided into four groups:control group,high glucose group,siRNA group and high glucose+siRNA group. Expression of p22phox,intracellular ROS level,and cell apoptosis in hUVEC were detected by Western-blot and flow cytometry respectively. Results p22phox-siRNA could induce NAD(P)H oxidase subunit p22phox gene silence,high glucose could induce p22phox expression. Compared with high glucose group,ROS level and cell apoptosis was decreased in high glucose+siRNA group(P<0.05). Conclusion Inhibiting p22phox expression could decrease ROS level and cell apoptosis induced by high-glucose.

Abstract:Aim To evaluate the impact of gene transfection of hypoxia inducible factor 1α to acute myocardial infarction of rat. Methods 72 healthy male Wistar rats weighting 250~350 g were divided into three groups:hypoxia inducible factor 1α gene transfection group (HIF-1α group),control goup and sham-operation group. Each group was divided into 3 d,7 d and 14 d subgroups; There are 8 rats in each subgroup. After the ligation of LCA,the total 50 μg plasmid HIF-1α and null plasmid were injected into the infarct zone at three locations in HIF-1α group and control group respectively. The sham-operation group did not undergo litigation of left anterior descending coronary. The mRNA expression of HIF-1α and capillary density were detected. The myocardial infarction size was measured. Results Capillary density increased significantly in HIF-1α group compared with the control group (P<0.01). The mRNA expression of HIF-1α increased significantly in HIF-1α group compared with the control group (P<0.01),while the myocardial infarction size decreased significantly (23.85%±2.25% vs 38.74±3.12%; P<0.01). Conclusion The gene transfection of hypoxia inducible factor 1α in myocardium of rat can reduce infarction size and enhance angiogenesis in acute myocardial infarction of rat.

Abstract:Aim Using a rabbit common carotid arteries balloon injury stenosis model,to observe the influence of proteasome inhibitor MG132 on vascular stenosis and expression of ubiquitin and caspase-3. Methods 30 New Zealand white rabbits were randomly divided into control group,the balloon injury group and MG132 group. After the rabbits were fed respectively for 8 weeks,their common carotid arteries were made pathology section. Ubiquitin and caspase-3 protein expression were measured by immunohistochemistry. Results The expression of ubiquitin protein was remarkably inhibited (P<0.01) and caspase-3 was up-regulated (P<0.01) by MG132. Conclusion The inhibitory effect on vascular stenosis of proteasome inhibitor MG132 may associate with interdicting ubiquitin-proteasome pathway and up-regulating caspase-3 expression.

Abstract:Aim To investigate the effect of water extract propolis on cholesteryl ester accumulation in human umbilical artery smooth muscle cell (HUASMC),and explore the mechanism of water extract propolis on inhibition of atherosclerosis and it's implications. Methods HUASMC was cultured by explant method,foam cell model derived from smooth muscle cell was prepared:coculturing HUASMC with ox-LDL in concentration of 25,50 and 75 mg/L respectively,the intracellular total cholesterol (TC)and free cholesterol(FC) at 12,24,36,48 and 60 h were measured by high performance liquid chromatogram,coculturing HUASMC with ox-LDL in concentration of 50 mg/L for 48 h as the optimum condition for foam cell formation. Cultured HUASMC were randomly divided into 5 groups:control group (without any drug),model group (50 mg/L ox-LDL for 48 h),propolis groups (50 mg/L ox-LDL and 50 mg/L,100 mg/L,200 mg/L WEP respectively for 48 h). Intracellular total cholesterol and free cholesterol were measured by high performance liquid chromatogram,the content of cholesterol ester (CE) was obtained by subtracting the FC from TC. Results HUASMC were cocultured with 50 mg/L ox-LDL for 48 h,the ratio of intracellular CE/TC was more than 50%,and the cells were transformed into foam cell. The content of intracellular CE in model group was more than that in the control group (P<0.01); The content of intracellular CE in 50 mg/L,100 mg/L and 200 mg/L WEP groups were less than that in the model group (P<0.01),and with the increase of the concentration of WEP the content of intracellular CE had the tendency of decreasing. Conclusion ox-LDL can induce the cholesteryl ester accumulation in cultured HUASMC in vitro,and transform it into foam cell,simultaneously it can raise the apoptosis index of HUASMC. WEP can reduce the extent of intracellular CE accumulation in HUASMC induced by ox-LDL,and that maybe one of the mechanisms of it's anti-atherosclerosis effect.

Abstract:Aim To study the association between serum adiponectin and insulin resistance in the type 2 diabetes mellitus patients with obesity,and investigate the role of serum adiponectin in the type 2 diabetes mellitus patients with obesity who had insulin resistance. Methods 30 T2DM patients with obesity,25 T2DM patients,and 25 controls which included 13 with obesity were selected. Their body mass index (BMI),waistline,fasting plasma glucose (FPG),hemoglobin a1c( HbA1c),fasting insulin (FINS) ,and the serum levels of total cholesterol,triglyceride and adioponectin were measured. Then the HOMA-IR and ISI were calculated. At last,the relationships between serum adioponectin and insulin resistance were analyzed. Results ⑴The BMI,HbA1c,FPG,HOMA-IR,FINS were significantly higher in diabetic obese group than control obese group,serum adiponectin and ISI was significantly lower in diabetic obese group(P<0.05). (2)The triglyeride,HbA1c,FPG,HOMA-IR,FINS were higher in diabetic group without obesity than control group without obesity,serum adiponectin and ISI was lower in diabetic group without obesity(P<0.05). (3)The triglyeride,cholesterol,HbA1c,FPG,HOMA-IR,FINS,waistline were higher in diabetic obese group than diabetic group without obesity,serum adiponectin and ISI was lower in diabetic obese group(P<0.05). Conclusion The serum adiponectin level were correlated with insulin resistance in obesity with type 2 diabetes mellitus patients. Lower adiponectin leads to insulin resistance.The level of adiponectin can serve as an indicator in detecting insulin resistance in type 2 diabetes mellitus patients with obesity.

Abstract:Aim To research the change of plasma soluble CD40 ligand (sCD40L) in the patients with coronary heart disease,and the influence of EXCEL stent on sCD40L. Methods 80 patients were divided into BMS group and EXCEL group according to different treatment from January 2006 to June 2008. 40 cases in each group were followed up by coronary artery angiography. The level of sCD40L was measured on 1,3 ,6 months after operation. Results The difference of the level of sCD40L was significant on 1,3 months after operation between the two groups (P<0.01),but no significant difference on 6 months (P>0.05). Conclusion EXCEL stent could reduce plasma sCD40L with proper endothelialization to decrease restenosis and delayed thrombosis.

Abstract:Aim To determine whether the degree of carotid atherosclerosis is associated with left ventricular hypertrophy(LVH) in maintenance hemodialysis(MHD) patients. Methods Thirty-six MHD patients were included in this study. Their biochemical parameters,including C-reactive protein before hemodialysis,creatinine,blood urea nitrogen (BUN),total cholesterol,haemoglobin,plasma albumin,calcium,phosphorus and parathormone were examined by routine methods. The anatomy,hemodynamics,atheromatous plaque and intima media thickness(IMT) of bilateral carotid artery,carotid bifuracation and carotid internal artery were measured by color Doppler. The left ventricular end-diastolic dimension,left atrium diameter,interventricular septum thickness at end diastole,left ventricular posterior wall thickness at end diastole,right ventricular outflow tract diameter,right ventricular diameter,stroke volume,cardiac output and left ventricular ejection fraction were also detected by ultrasonic cardiography. The left ventricular mass index was calculated as well. Results The plaque-positive was detected in 24 of the patients (67%). The plaque-positive patients had elder age,longer dialysis time,more C-reactive protein,lower plasma albumin(P<0.05). And the plaque-positive patients had higher intima media thickness of carotid,interventricular septum thickness at end diastole and left ventricular mass index. Conclusion The carotid atherosclerosis is associated with LVH in MHD patients. Whether the treatment of atherosclerosis may cause regression or even prevent LVH in MHD patients remains to elucidate.

Abstract:Aim To evaluate the clinical efficacy of the treatment of acute cerebral hemorrhage of edaravone injection. Methods 86 patients with acute cerebral hemorrhage were randomly divided into observation group (n=46) and control group (n=40). The two groups were given conventional therapy,but the observation group added with intravenous infusion edaravone for four weeks. Neurologic impairment score,daily life activites ability score,hematoma volume and edema volume were observed. Results The differences of decrease of neurologic impairment score after 4 weeks treatment and the improvement of daily life activities ability score after 2 and 4 weeks treatment of the observation group were statistically significant compared with control group (P<0.05); the differences of hematoma volume after 4 weeks treatment and the edema volume after 2 and 4 weeks treatment of the observation group were statistically significant compared with the control group (P<0.05); the total efficiency of the observation group after 4 weeks treatment was higher than that of control group (P<0.05). The occurrence rate of the two group adverse events were the same. Conclusion Edaravone is a safe and effective drug to the treatment of acute cerebral hemorrhage,which can improve neurologic impairment and the level of activities of daily life of the patients with acute cerebral hemorrhage,and promote hematoma absorption and restrain edema formation.

Abstract:Aim To study the the therapeutic efficacy and safety of amlodipine in the therapy for renal hypertension. Methods 76 patients of renal hypenension with chronic renal failure were diagnosed to be treated with amlodipine for 12 weeks and compared with captopril. The initial dose was 5 mg Q12h,the maximal dose was 10 mg Q12h. the captopril dose was 25 mg Q 8h. The blood pressure,renal function,urea protein,heart rate,administration status and adverse reactions of the patients were observed during treating time. Results After 12 weeks of treatment,the blood pressure in amlodipine group was reduced by(23.00±5.28)/(19.29±2.31) mmHg. The total effective rate in amlodipine group 92.11%(70/76) respectively. The total adverse incidence rate in amlodipine group was 9.21%(7/76).While the blood pressure in captopril group was reduced by(11.90±4.18)/(11.80±2.29) mmHg. The total effective rate in captopril group was 61.67%(37/60) respectively. The total adverse incidence rate in captopril group were 16.67%(10/60). There were no obvious changes of heart rate and renal function after treatment and no obvious adverse event was showed in amlodipine group. Conclusion Amlodipin has a better eficacy and is safe in the therapy of chronic renal failure patients with renal hypertension.

Abstract:Aim To observe the therapeutic effect and cadiovascular adverse reaction of rh-endostatin injection (YH-16,Endostar) combined with paclitaxel and cisplatin on advanced non-small-cell lung cancer(NSCLC). Methods Endostar combined with paclitaxel and cisplatin were administrated to 43 advanced non-small-cell lung cancer cases of stage Ⅲ-Ⅳ. Every course lasted 3 weeks,and all cases were evaluated after 2 courses at least; and safety was evaluated after one course. Results The objective response rate (ORR) was 48.79% (21/43) and disease control rate (DCR) was 81.4 % (35/43),1-year overall survival rate was 51.2%,median survival time was 12.2 months. The quality of life (QOL) were improved on 29 cases (67.44%),decreased on 6 cases (6/43). The occurrence rates of G3/4 toxicities were low,including neutropenia (11.63%,5/43),thrombocytopenia (6.98%,3/43),nausea/vomiting (4.65%,2/43). These toxicities were mainly related with the chemotherapy agents. Conclusion Endostar combined paclitaxel and cisplatin as the first line on advanced non-small-cell lung cancer is highly effective and safe. The QOL of patients with advanced lung cancer may be improved by endostar combined with the paclitaxel and cisplatin chemotherapy. It indicates that endostar has synergetic effects on some of cytotoxic agents or reverses tumor drug resistance such as paclitaxel and cisplatin. It is worthy of clinical generalization and further clinical observation.

Abstract:Aim To investigate the clinical features,laboratory examination,risk factors of coronary artery lesions and treatment for atypical kawasaki disease. Methods A total of 55 patients with atypical kawasaki disease were reviewed. Results In this group of cases,persistent fever(100%),bulbar conjunctiva congestion(54.5%),the change of lip and mouth(72.7%)、the end of hand and foot being hard and swollen (63.6%),Skin rash(29.1%)and the limphs in neck swelling(30.9%) had significance in early diagnosis of atypical kawasaki disease (KD),in addition,flush or exuviation around the anus (58.2%) and BCG vaccination scar being red and swollen (52.7%) also had reference significance. In laboratory target,erythrocyte sedimentation rate markedly increased(69.1%),C response protein obviously went up(56.4%) and platelets remarkably increased (49.1%) or white blood cells evidently increased(60%),so these could give assistance in the diagnosis of atypical kawasaki disease (KD). At the same time,it should be as early as possible to apply echocardio graphy. 12 cases were complicated with coronary artery lesions,including 11 coronary artery dilations,1 coronary artery aneurysms. The patients with coronary artery lesions were followed up from 6 months to 18 months,and 12 cases regressed completely. Conclusion It is necessery to enhance the vigilance of atypical kawasaki disease,consummate the correlation inspection promptly,make clear about the diagnosis and the treatment as soon as possible to reduce the coronary artery damage.

Abstract:The renin angiotensin system (RAS) is emerging as a prominent factor in the development of experimental atherosclerosis. We have previously demonstrated that the RAS is profoundly activated in hypercholesterolemia. This was demonstrated in LDLR-/-mice fed a saturated fat enriched diet and manifested as increased plasma concentrations of angiotensinogen and angiotensin peptides; especially angiotensin Ⅱ(AngⅡ).

Abstract:Death due to cardiovascular diseases including those related to atherosclerosis,particularly myocardial infarction,and cerebrovascular accidents,particularly cerebral infarction and stroke,have accounted for a high percentage of death cause,reaching 30%,along with cancer in the mortality statistics of Japanese.

Abstract:Background Cardiovascular disease (CVD) is mainly caused by atherosclerosis,for which dyslipidemia (i.e. high (V)LDL-cholesterol (C),high triglycerides and low HDLC is a major risk factor. To reduce the risk to develop CVD,patients with dyslipidemia are usually treated with lipid-lowering drugs including statins and fibrates.

Abstract:Plant derived phospholipids are rich in linoleic acid (LA) and have therapeutic value to treat inflammatory diseases of the liver,intestine and vasculature. These phospholipids act to normalize plasma lipid levels and prevent atherosclerotic disease. Oral administration of LA-phospholipids to cholesterol-fed rabbits prevents the development of atherosclerosis.

Abstract:High levels of plasma high-density lipoproteins (HDL) are associated with a low incidence of cardiovascular disease[1]. HDL contains two major apolipoproteins (apo):apoAI and apoAII. It is generally accepted that apoAI plays a central role in reverse cholesterol transport and protects against atherosclerosis[2,3]; however,apoAII functions have not been clearly characterized[4-6].

Abstract:Platelets are anucleate cells generated from megakaryocytes in the bone marrow. After being released into the blood,platelets play essential roles in hemostasis and preserving vessel wall integrity. However,the processes of platelet adhesion,activation,and aggregation at the site of vascular injury may also cause vessel occlusion,and lead to thrombotic diseases.

Abstract:Stem-cell therapy may provide a novel therapeutic strategy for cardiovascular diseases as well as other degenerative diseases. A rapid transition from animal research to clinical trials is taking place. However,numerous issues remain unresolved,particularly the molecular mechanisms underlying potential therapeutic benefits of stem cells.

Abstract:Atherosclerosis is an inflammatory disease characterized by leukocyte infiltration,smooth muscle cell accumulation and neointima formation[1]. Activation and damage of the endothelial monolayer seems to trigger the development of the lesions. Initially,it was thought that the damaged endothelial cells were replaced by the adjacent intact endothelium.

Abstract:The metabolic syndrome is strongly associated with insulin resistance and consists of a constellation of factors such as hypertension and hyperlipidemia that raise the risk for cardiovascular disease (CVD) and diabetes mellitus. Emerging data suggest that peroxisome proliferator-activated receptor-γ(PPARγ) is a critical determinant that may provide functional links between diabetes and CVD.

Abstract:Endothelial progenitor cells (EPC) are the precursors of mature endothelial cells and are involved in neovascularization and reendothelization. Previous studies have shown that oxidative stress can induce EPC senescence. However,the potential molecular mechanisms involved are still not clearly elucidated.

Abstract:Aim To investigate the differentiation of marrow stromal cells induced by low density lipoprotein(LDL) into smooth muscle-like cells and the role of myocardin in it. Methods Bone marrow stromal cells(BMSC) of mouse were purified by disparation adherence technique.The cultured BMSC were divided into 4 groups: regular culture group,regular culture+LDL group(LDL 25 mg/L),20% fetal bovine serum(FBS) culture group,20% FBS culture+LDL group.The expression of myocardin,α-SMA and SM-MHC were detected by immunocytochemistry technique.RT-PCR was used to detect the mRNA expression of myocardin,α-SMA and SM-22α. Results It is showed by immunocytochemistry that the expression of myocardin,α-SMA and SM-MHC expressed in regular culture+LDL group(LDL 25 mg/L),20% fetal bovine serum(FBS) culture group,20% FBS culture+LDL groups were signifcnatly higher than that in regular culture group(P<0.05).The expression of the three proteins in 20% FBS culture+LDL group were significantly higher than that in 20% fetal bovine serum(FBS)group(P<0.05).The proteins expression of α-SMA(r=0.9018,P<0.05) and SM-MHC(r=0.7969,P<0.05) were positively related with myocardin.It is approved by RT-PCR that the mRNA expression of myocardin,α-SMA and SM-22α in regular culture+LDL group(LDL 25 mg/L) 20% fetal bovine serum(FBS),20% FBS culture+LDL group.groups were significantly higher than that in regular culture group(P<0.05).The mRNA expression of the three genes in 20% FBS culture+LDL group were significantly higher than that in 20% fetal bovine serum(FBS) group(P<0.05).The mRNA expression of α-SMA(r=0.9295, P<0.05) and SM-22α(r=0.8940,P<0.05) were positively related with myocardin. Conclusion Both 20% FBS and LDL could induce the differentiation of BMSC into smooth muscle-like cells.The role of LDL with 20% FBS inducing the differentiation of BMSC into smooth muscle-like cells was the strongest.And myocardin may play an important role in this differentiated process.

Abstract:Aim To investigate the effects of advanced glycation endproducts(AGE) on oxidative stress in bone-marrow derived endothelial progenitor cells(EPC) and the relationship of EPC functions. Methods Mononuclear cells(MNC) were isolated from rat bone marrow by Ficoll density gradient centrifugation and cultured for 7 days,EPC were identified as adherent cells double positive stained for FITC-UEA-Ⅰand DiI-acLDL under laser confocal immunofluence microscope.EPC were cultured in the absence or presence of AGE(50,100 and 200 mg/L).Reactivated oxygen species(ROS) were analyzed using the ROS assay kit.A spectrophotometer was used to assess superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) expression,and the PCR was also used to determine the mRNA expression.A modified Boyden's chamber was used to assess the migration of EPC and the number of recultured EPC was counted to measure the adhesiveness function.A spectrophotometer was used to determine the proliferation function. Results Co-culturing with AGE increased ROS production,decreased antioxidase and induced the proliferation,migration and adhesion of EPC inhibition in a dose dependent manner. Conclusion AGE increase oxidative stress and mediate impairment of progenitor cell function in a dose dependent manner,which indicates a new pathophysiological mechanism of disturbed vascular adaptation in atherosclerosis and suggests that lower levels of AGE might improve the success of progenitor cell therapy.

Abstract:Aim To investigate the effects of advanced glycation end products(AGE) on calcification in cultured rat aortic vascular smooth muscle cells(VSMC). Methods To induce calcification,VSMC were treated with 10 mmol/L β-glycerophosphate(β-GP) with the indicated concentrations of AGE-BSA or non-glycated BSA for various periods of time.Calcium deposition,the activity and mRNA expression of alkaline phosphatase(ALP),as well as core band factor α-1(Cbfα-1) and osteopontin(OPN) were used to identify osteoblastic differentiation and mineralization in VSMC induced by AGE-BSA. Results AGE increased calcium deposition in VSMC in time-and dose-dependent manners.Mechanistic studies revealed that elevated AGE treatment of VSMC enhanced the activity and mRNA of alkaline phosphatase,as well as the expression of Cbfα-1 and its downstream protein osteopontin. Conclusion The results suggest that AGE accumulated in diabetes could elicit the osteoblastic differentiation of VSMC,thereby contributing to vascular calcification.

Abstract:Aim To explore whether adipophilin affects the expression of acyl-coenzyme A∶cholesterol acyltransferase 1(ACAT1) and illuminate the lipid-accumulation mechanism mediated by adipophilin. Methods The recombinant retroviral vector pQCXIP-HA-Adi was constructed and transfected into packaging cell PA317 mediated by SofastTM,which can induce retrovirus release.Then this retrovirus were used to infect RAW264.7 cell and got RAW264.7 cell line which highly expressed adipophilin.The mRNA level of adipohilin and ACAT1 was determined by reverse transcription-polymerase chain reaction(RT-PCR).The adipophilin and ACAT1 proteins were analyzed by Western blotting.After that,the cells were incubated with atorvastatin for investigating the expression of ACAT1 again. Results After infecting with the retrovirus,both adipophilin mRNA and protein up-regulated,so did ACAT1. However,no effect on ACAT1 expression was found in blank virus transfected cells.The expression of ACAT1 still increased in high-adipophilin-expression cells after using atorvastatin to inhibit endogenous cholesterol synthesis and starving to inhibit exogenous cholesterol. Conclusion Overexpressed adipophilin upregulated ACAT1 expression in RAW264.7 cells.

Abstract:Cardiovascular disease are related to arrhythmias and heart failure.A established Drosophila model for studying heart failure which provides a faster and more accurate method for a large-scale screening of heart failure-related genes in different fruit fly chromosomes may laid foundation for the further study of the pathogenesis of human cardiovascular disease.In this paper,the heart failure rate of 53 deficiency lines in the first chromosome have been studied by the model.Nine deficiency lines which show a prominent cardiac failure phenomenon have been identified that are related to the occurrence of heart failure.

Abstract:Aim To explore the influence of angiotensin-(1-7) [Ang-(1-7)] on the secretion of E-selectin(E-sel) and monocyte chemotactic protein-1(MCP-1) in cultured human umbilical vein cells induced by angiotensin Ⅱ(AngⅡ),and to clarify the antagonism of Ang-(1-7) on the inflammation induced by AngⅡ. Methods The cultured human umbilical vein endothelial cells(HUVECs) were randomly divided into control group,AngⅡ group,Ang-(1-7) group,Ang-(1-7)+AngⅡ group,and A-779+Ang-(1-7)+AngⅡ group.The expressions of E-sel and MCP-1 inprotein level and mRNA level were detected by enzyme linked immunosorbent assay(ELISA) and reverse transcription polymerase chain reaction(RT-PCR). Results ①Compared with the control group,100 nmol/L AngⅡ distinctly increased the protein of E-sel(25.39±1.97 μg/L) and MCP-1(238.71±5.51 ng/L) in HUVECs(P<0.01),and significantly increased mRNA expression of E-sel and MCP-1 in HUVECs(P<0.01).②Compared with the AngⅡ group,Ang-(1-7)(1 000 nmol/L) decreased the protein of E-sel(3.72±0.95 μg/L) and MCP-1(90.24±9.82 ng/L)(P<0.01),and the mRNA expression of E-sel and MCP-1(P<0.01).③10～10 000 nmol/L Ang-(1-7) attenuated the protein of E-sel in HUVECs induced by AngⅡ in a concentration dependent manner(21.15±1.31 μg/L,17.41±1.94 μg/L,12.71±1.84 μg/L and 9.46±1.40 μg/L)(P<0.01),and also inhibited the protein of MCP-1 in HUVECs induced by AngⅡ in a concentration dependent manner(214.57±7.16 ng/L,196.83±8.20 ng/L,176.63±8.93 ng/L and 155.52±8.19 ng/L)(P<0.01).④Compared with the AngⅡ group,10～10 000 nmol/L Ang-(1-7) inhibited the mRNA expression of E-sel and MCP-1 in HUVECs induced by AngⅡ in a dose dependent manner(P<0.01).⑤The A-779 group had no significant deviation than the AngⅡ group(P>0.05). Conclusions Ang-(1-7) inhibited the secretion of E-sel and MCP-1 in cultured HUVECs induced by AngⅡ in a concentration dependent matter.The inhibition effect of Ang-(1-7) may be through its specific receptor.

Abstract:Aim To study the distribution,correlation and its significance of CD68-positive macrophages with the coronary atherosclerotic lesion types and luminal stenosis in human coronary atherosclerotic lesions. Methods 312 of coronary artery tissue samples were selected in 53 caes of autopsy.Coronary atherosclerotic lesion and its types were diagnosed by light microscope,and in coronary atherosclerotic lesions,CD68-positive macrophages were counted by using immunohistochemistry,and the degree of lumen stenosis,area of lipid necrotic core and calcifying matrix were detected and calculated by using the Scion image software systems. Results Area of lipid necrotic core was significantly greater in the high cholesterol group than in the normal cholesterol group(P<0.05),and area of calcifying matrix was significantly different between the early lesions(typeⅠ～Ⅲ) and advanced lesions(typeⅣ～Ⅵ;P<0.05).CD68-positive macrophages in coronary atherosclerotic lesions were increased with progress of coronary atherosclerotic lesions and aggravation of luminal stenosis,and positive correlation(P<0.01),respectively,and had significant differences among lesion types,and degree of luminal stenosis as well as between normal cholesterol and high cholesterol groups(P<0.05). Conclusions CD68-positive macrophages in coronary atherosclerotic lesions are increased with progress of coronary atherosclerotic lesions and aggravation of luminal stenosis,indicating that infiltration of CD68-positive macrophage initiates and aggravates the coronary atherosclerotic lesions,and a large number of macrophages mainly infiltrated in the shoulder area and increased lipid necrotic core of plaque,which are associated with progress of coronary atherosclerotic lesions,unstable plaque rupture,and the occurrence of complications in coronary atherosclerosis.

Abstract:Aim To research the expression level of scavenger receptor BⅠ(SR-BⅠ) in endothelial cells under low laminar shear stress,and to investigate the possible role of SR-BⅠ on the formation of atherosclerosis. Methods The fresh fetal umbilical cord were taken from the health parturient women,and the human umbilical vein endothelial cell(hUVEC) were cultured.The second to fourth generations of endothelial cells will be used in the experiment and then the endothelial cells were planted on the glass slide.After the cell covering the glass slide completely,the glass slide was put in the flow chamber system.The endothelial cells was dealt with different shear stress: the control group was not dealt with shear stress,the dealt group was dealt with the low shear stress(4.2 dyne/cm2).The two groups were treated for 1 h,2 h,4 h and 8 h.Taking the glass slide out of the flow chamber system,total RNA was extracted and the expression level of the SR-BⅠ was detected with RT-PCR and agargel electrophoretic analysis according to the operation instruction of the RT-PCR box. Results The expression of SR-BⅠ became weaker and weaker when it was stimulated continuously by the low shear stress(4.2 dyne/cm2),the lowest expression of SR-BⅠ was at the 8 h,and it almost didn't appear in the electrophoresis picture. Conclusion The expression of SR-BⅠ decreased when it was treated by low shear stress.The harmful mechanism of the low shear stress is that it can reduce the anti-transfer of the cholesterin through decreasing the expression of the SR-BⅠ,and increase the incidence of atherosclerosis.

Abstract:Aim To study the effect and possible mechanism of nicorandil postconditioning on myocardial ischemia reperfusion(MIR) injury in rats. Methods The SD rats were randomly divided into six groups: control group,ischemia reperfusion group,postconditioning group,nicorandil postconditioning groups of 2 mg/kg,5 mg/kg,and 10 mg/kg.Ischemia reperfusion group was obtained by ligated left anterior descending coronary artery 30 minutes and followed by 120 minutes reperfusion.Postconditioning group was obtained by 5 cycles of brief 10 seconds intermittent reperfusion/reocclusion.After 30 minutes ischemia,hearts were exposed to nicorandil for 10 minutes immediately at the onset of reperfusion.Contents of creatine kinase(CK) and malondialdehyde(MDA),activity of superoxide dismutase(SOD) were detected respectively.Apoptosis rates and the expression of caspase-3 were investigated. Results In the nicorandil postconditioning groups,contents of CK and MDA were lower,activities of SOD were higher,apotosis rates were decreased,and caspase-3 was lower. Conclusions Nicorandil postconditioning could protect MIR.The myocardial protective mechanism maybe realized by enhancing the activity of SOD,enhancing myocardial antioxygen capability,reducing the oxygen free radical injury,stabilizing myocardial cellular membrance and inhibition of apoptosis.

Abstract:Aim To evaluate the effect of AngiotensinⅡon EMMPRIN expression in THP-1 macrophage and its potential mechanism. Methods Macrophages cell line was esteblished by induced THP-1 using PMA,and then the effect of AngⅡ on EMMPRIN expression on THP-1 macrophages was investigated. Results RT-PCR and Western Blot showed that AngⅡ upregulated EMMPRIN expression in a dose and time dependent manner.Either nuclear factor-κB inhibitor PDTC or P65 RNAi treatment can suppress the effect of angⅡon EMMPRIN. Conclusion AngⅡupregulates the expression of EMMPRIN.Nuclear factor-κB is the critical factor involving in the EMMPRIN upregulation induced by angⅡ.

Abstract:Aim To study the effects of heat shock pretreatment on the lipopolysaccharid-induced macrophage migration. Methods The effect of lipopolysaccharid on the release of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in murine macrophage-like RAW264.7 cells were detected by ELISA;the effect of lipopolysaccharid on the migration of RAW264.7 macrophages were detected by chemotaxis assay;the effect of heat shock pretreatment on the migration of RAW264.7 macrophages were detected by chemotaxis assay. Results Interfered with 500 μg/L lipopolysaccharid for 1 h,the release of TNF-α and IL-1β were significantly increased(P<0.05) in RAW264.7 macrophages;interfered with 500 μg/L lipopolysaccharid for 24 h,the migration of RAW264.7 macrophages was significantly increased(P<0.05);given a heat shock pretreatment about 42.5℃ for 1 h followed with the interference of 500 μg/L lipopolysaccharid,the migration of RAW264.7 macrophages induced by lipopolysaccharid was significantly inhibited(P<0.05). Conclusion Heat shock pretreatment significantly inhibited lipopolysaccharid-induced macrophage migration.

Abstract:Aim To investigate changes of serum nitric oxide(NO) in stroke-prone renovascular hypertensive rats(RHRSP) before artificicial cold.To explore the possibility of nitric oxide used as the prediction index of stroke. Methods Two-kidney,two-clip methods were used to copy the model of renovascular hypertension in rats,Serum NO levels were measured by nitrate reductase before and after artificicial cold. Results Serum NO levels in cerebral infarction group and cerebral hemorrhage group were significantly lower than that in the non-stroke group before artificicial cold;serum NO levels in cerebral infarction group and cerebral hemorrhage group after artificicial cold were significantly lower than that before artificicial cold. Conclusion Serum NO could be used as the prediction index of stroke.

Abstract:Aim To explore the relationship between blood pressure and carotid haemodynamics in normotensive carotid stenosis patients by color duplex ultrasonography. Methods The 80 mortotensive carotid stenosis patients were checked for the blood pressure and carotid haemodynamics indexes,including systolic blood pressure(SBP),diastolic blood pressure(DBP) and the haemodynamics premeters of blilateral carotid arteries. Results The stenosis grades would accelerate blood velocity of the stenosis internal carotid artery.The vertebral artery blood flow velocity were faster in SBP of 90 to 120 mmHg and DBP of 60 to 79 mmHg,while the blood flow resistance was smaller in the same blood pressure level.Then the vertebral artery blood flow velocity would go down and the blood flow resistanc would raise,with the increase of blood pressure especially SBP of >120 mmHg,DBP of ≥80 mmHg. Conclusion Lowering blood pressure could help promoting the carotid blood flow velocity and increasing cerebral blood flow.And SBP of 90 to 120 mmHg and DBP of 60 to 79 mmHg may help maintaining the better cerebral haemodynamics.

Abstract:Aim To investigate the association of metabolic syndrome(MS) with aortic stiffness according to different definitions in continuous ambulatory peritoneal dialysis(CAPD) patients,in order to find a suitable criterion for CAPD population.At the same time,to analyze the risk factors affecting aortic stiffness. Methods 155 CAPD patients were studied.Arterial stiffness was assessed by measuring carotid-femoral pulse wave velocity(PWV).Metabolic syndrome was defined by Adult Treatment Panel(ATP) Ⅲ2001,World Health Organization(WHO)1999,and International Diabetes Federation(IDF) 2007 criteria. The PWV values were compared between MS group and non-MS group,and the risk factors associated with PWV were analyzed. Results By all definitions,which include WHO 1999,IDF2007 and ATPⅢ 2001 definition,CAPD patients with MS had higher PWV compared to CAPD without MS(P<0.05).An independent association emerged between PWV and age,waist circumference,systolic blood pressure,serum glucose positively(P<0.05 or P<0.01).And PWV was associated with serum high density lipoprotein cholesterol negatively and independently in CAPD patients(P<0.05). Conclusions Arterial stiffness is increased in CAPD patients with metabolic syndrome irrespective of the definition criteria,which includes WHO 1999,IDF 2007,ATPⅢ 2001 criterion.Age and metabolic components affect arterial stiffness independently.Based on all considerations,the ATP criterion of MS was proposed for CAPD patients.

Abstract:Aim To evaluate the relation between the systolic blood pressure and carotid atherosclerosis in older hypertensive patients. Methods 120 cases of older hypertensive patients were selected from May 2007 to October 2008.These patients were divided into 2 groups.There were 60 cases with isolated systolic hypertension in the first group and 60 cases with non-isolated systolic hypertension in the second group.Then the degree of carotid atherosclerosis was compared between two groups through ultrasonic testing. Results There were significant differences in incidence of carotid intima-media thickening and atherosclerosis between isolated systolic hypertensive group and non-isolated systolic hypertensive group. Conclusion The systolic blood pressure indicates stronger signification than the diastolic blood pressure in atherosclerosis.

Abstract:Aim To determine the clinical value of serum visfatin,as well as to investigate the relationship between the serum level of visfatin and the severity of coronary artery disease(CAD) combined with high sensitive C-reative protein(hs-CRP). Methods All the subjects underwent coronary angiography and serum visfatin,creatine kinase MB isoenzyme(CK-MB),cardiac troponin-Ⅰ(cTnⅠ) and hs-CRP were measured in the subjects.According to diagnostic results,all cases were divided into two groups,normal control group(25 cases) and CAD group(78 cases).At the same time,the 78 cases of CAD were divided into three groups,34 cases of stable angina pectoris(SAP),20 cases of unstable angina pectoris(UAP),24 cases of acute myocardial infarction(AMI).Then CAD group were divided into 24 cases of single vessel coronary disease(1 branch) and 54 cases of multivessel coronary disease(≥2 branches or left trunk).The levels and relationship of serum visfatin and hs-CRP among these groups were compared and analyzed. The relationship between the severity of CAD and the two indicators was evaluated. Results The levels of serum visfatin and hs-CRP in the group of CAD were higher than those of normal control group.The levels of serum visfatin and hs-CRP in the UAP group were higher than that in SAP group(P<0.05),which in the AMI group were higher than that in UAP group(P<0.05).There was no significant correlation between serum visfatin and hs-CRP levels(P>0.05).In the 78 cases of CAD,there was no significant difference of serum visfatin levels between multivessel coronary disease group and single-vessel coronary disease group(P>0.05),but the levels of serum hs-CRP in multivessel coronary disease group were higher than those in single-vessel coronary disease group. Conclusion The increased serum levels of visfatin and hs-CRP in patients with CAD may predict the unstable conditions of plaques.Hs-CRP plays a role in predicting the severity of CAD to some extent.But we should not predict the severity of CAD by the level of serum visfatin.