Abstract:Aim To create an animal model for local change of shear stress to analyze the arterial wall response at different patterns of fluid shear stress. Methods 24 mice were equally randomized into three group (1 h group,4 h group and 24 h group) and one normal control group. A stenosis was set up with a cast attached to the wall of the abdominal aorta to change flow condition in test group. The parameters of hemodynamics and the internal diameter of blood vessel were measured by color Doppler flow imaging. The wall shear stress was calculated by Poiseiulle hydrodynamics formula (τm=η×4×Vm/D). Pathological examination and immunohistochemistry were performed to observe the arterial morphological changes and the endothelial P-selectin expression. The intimal-media thickness and adventitia thickness of the aorta were measured and endothelial P-selectin expression intensity was analyzed qualitatively. Results Regions of low shear stress and oscillatory shear stress were created upstream and downstream of the cast respectively. Vascular remodeling and P-selectin expression in the upstream arterial wall were much more severe than those in the downstream in all observed time-points (P><0.05). Conclusion Vascular remodeling and endothelial P-selectin expression could happen in a relative short time when it exposed under low shear stress,meanwhile the variant patterns of fluid shear stress may play different roles in the pathological process of artery.

Abstract:Aim To investigate the influence of carbon monoxide(CO)/heme oxygenase-1 (HO-1) system on neointimal proliferation and endothelium function. Methods Fifty rabbits were randomly divided into 5 groups of 10 rabbits. Control group received normal chow(C group),the other rabbits received 1.5% cholesterol diet (Ch group and SH group) or 1.5% cholesterol diet plus hemin (Hm group) or zincprotoporphyrin IX (Zn group) for 10 weeks. At the beginning of 3rth week,Ch group,Hm group and Zn group underwent balloon injury at one side carotid artery. Results High cholesterol diet markedly enhanced the levels of serum TC,TG,LDLC and ox-LDL (P><0.01). However,they were not much different among these four experimental groups. Compared with control group,arterial NO production and cNOS activity decreased markedly,while CO production and HO activity increased markedly(all P><0.01),the intima area and ratio of intima/media (I/M) were respectively 0.586±0.090 vs 1.381±0.180 in Ch group. Compared with Ch group,CO production and HO-1 activity increased markedly in Hm group,while in Zn group they were decreased markedly. Compared with Ch group,arterial endothelin-1(ET-1) level of Hm group reduced markedly while in Zn group they were significantly higher than Ch group. The intima area and ratio of I/M were reduced distinctly in Hm group (respectively 0.386±0.076 vs 0.862±0.164) while they were distinctly increased in Zn group (respectively 0.734±0.096 vs 1.843±0.212). Conclusion Arterial NOS/NO system is impaired significantly in atherosclerotic rabbits induced by highcholesterol diet and balloon injury.HO-1/CO system plays a key role in improving endothelium function and inhibiting neointimal proliferation. This role is related to the reciprocal relationship between HO-1/CO and NOS/NO system in restenosis and the down-regulated expression of ET-1.

Abstract:Aim To study the expression and significance of cathepsin B and Cystatin C in vascular smooth muscle cells (VSMC) of patients with abdominal aortic aneurysms (AAA) and to investigate underlying roles in pathogenesis of AAA. Methods 21 cases of AAA and 8 cases of normal abdominal aortas were collected in this study. HE staining and immunohistochemical technique were used to evaluate the change of cathepsin B and Cystatin C in the media of AAA. Results Immune reaction of cathepsin B was positive in the AAA,and immune reaction of Cystatin C was positive in the normal abdominal aortas. The positive cells were mainly localized in the smooth muscle cell (SMC). Imagine analysis results showed that the MOD value of cathepsin B in SMC of AAA evidently increased,while Cystatin C evidently decreased. There were significant differences in cathepsin B and Cystatin C between the AAA and normal abdominal aortas. Conclusion The expression of cathepsin B promoted and expression of Cystatin C reduced in the SMC of AAA. An imbalance between cysteine cathepsins and their inhibitor may cause the excessive breakdown of extracellular matrix (ECM) in the arterial walls leading to the progression and rupture of AAA.

Abstract:Aim To explore the effect of monocyte chemoattractant protein-1 (MCP-1) in viral myocarditis(VMC) and the change of MCP-1 after astragaloside intervention. Methods Fifty-five male 4-week-old Balb/c mice were randomly divided into 4 groups:normal control group (n=10),model control group (n=15),low-dose intervention group (n=15) and high-dose intervention group (n=15). Mice in the latter three groups were inoculated with 0.1 mL coxsackie B3 virus intraperitoneally. Then,mice in low-dose and high-dose intervention groups were treated with 0.01 g/L and 0.09 g/L astragaloside solution,respectively. Mice in normal control group and model control group were treated with carboxymethycellulose solution. All mice were killed on day 15. Histological cross sections of heart were stained with hematoxylin-eosin and myocardial histopathologic scores were counted under optical microscope. The expression levels of myocardial MCP-1 mRNA and protein were detected by RT-PCR and immunohistochemistry. Results The mortality was 0,46.7%,40.0% and 13.3% in normal control group,model control group,low-dose intervention group and high-dose intervention group respectively. Compared with model control group and low-dose intervention group,the mortality was significantly lower in high-dose intervention group (P><0.05). The expression levels of MCP-1 mRNA and protein for model control group were markedly higher than those of normal control group(P><0.01). However,the expression cevels of MCP-1 mRNA and protein and myocardial histopathologic scores in high-dose intervention group were decreased markedly compared with model control group and low-dose intervention group (P><0.05 or 0.01). Conclusion MCP-1 may participate in the pathogenesis of VMC. The therapeutic effect of Astragaloside on VMC is associated with inhibiting MCP-1 expression.

Abstract:Aim To investigate the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on platelet-derived growth factor (PDGF)-induced cardiac fibroblast proliferation and collagen synthesis,and the expression of JNK. Methods Neonatal rat cardiac fibroblasts were used in the experiment,the proliferation of cardiac fibroblasts was observed by MTT assay,the expression of typeⅠand type Ⅲ collagen protein in cardiac fibroblasts was detected by immunocytochemistry assay. The expression of JNK protein,phosphorylation of JNK protein and typeⅠand type Ⅲ collagen protein in cardiac fibroblasts was measured by Western Blotting analysis. Results 10 μg/L PDGF increased cell metabolic activity,expression of type Ⅰ and type Ⅲ collagen and phosphorylation of JNK,while the protein levels of JNK were not changed. 10-9 mol/L AcSDKP could inhibit cardiac fibroblasts proliferation,expression of type Ⅰ and type Ⅲ collagen and phosphorylation of JNK mediated by PDGF,while the protein levels of JNK were not significantly changed. Conclusion AcSDKP could inhibit the proliferation and collagen synthesis of cardiac fibroblasts induced by PDGF through blocking activation of JNK pathway.

Abstract:Aim To explore the effects of lisinopril on the activities of Na+,K+-ATPase and Ca²⁺+-ATPase and mRNA expression levels of Na+,K+-ATPase α1-subunit and plasma membrane Ca²⁺+-ATPase isoform 1(PMCA1) in cultured thoracic aorta vascular smooth muscle cells (ASMC) isolated from spontaneously hypertensive rats (SHR). Methods ASMC were divided into four groups:Wistar-Kyoto (WKY) control,SHR control,Lisinopril(1×10-6)intervened SHR group and lisinopril(1×10-5)intervened SHR group. The activities of ion pumps were detected by spectrophotography and mRNA expression were measured by real time PCR. The content of angiotensin Ⅱ(AngⅡ) in cells-cultured medium were detected by radioimmunoassay. Results The activities of Na+,K+-ATPase,Ca²⁺+-ATPase and the mRNA expression levels of Na+,K+-ATPase α1-subunit and PMCA1 in ASMC from SHR were significantly lower than those from WKY control (P><0.01). Lisinopril significantly increased the activities of Na+,K+-ATPase and Ca²⁺+-ATPase and mRNA expression levels of Na+,K+-ATPase α1-subunit and PMCA1 in ASMC from SHR (P><0.01). AngⅡcontent of culture medium in ASMC from SHR was significantly more than those from WKY control(P><0.05),lisinopril attenuated AngⅡcontent of ASMC culture medium from SHR (P><0.05). Conclusion The decreased activities of Na+,K+-ATPase and Ca²⁺+-ATPase may be related to their lower expression of the mRNA in ASMC from SHR. The lisinopril may increase the activities of two ion pumps and upregrulae the mRNA expression of Na+,K+-ATPase α1-subunit and PMCA1 in ASMC from SHR through blocking the generation of AngⅡ.

Abstract:Aim To investigate the protective effects of isorhamnetin against oxidized low density lipoprotein (ox-LDL) induced apoptosis of endothelial cells and to figure out some of the underlying mechanisms of these effects. Methods Changes in cell viability were measured by the MTT method,the lactate dehydrogenase (LDH) release was evaluated by assay kits,and nitric oxide (NO) release was detected by the Griess assay. JC-1 staining was used to evaluate the mitochondrial membrane potential alteration,AO/EB staining was used to observe the morphological changes of apoptotic cells,and flow cytometry was employed to detect the apoptotic rate of the cells. RT-PCR was used to detect the lectin-like low density lipoprotein receptor-1 (LOX-1) and Caspase-3 mRNA expression. Results With the pretreatment by isohamnetin (10-7 μmol/L,10-6 μmol/L and 10-5 μmol/L),the decrease in endothelial cell viability and NO release as well as the increase in LDH induced by ox-LDL were significantly suppressed (P><0.05). The ox-LDL-induced mitochondrial membrane potential alteration and apoptosis were also considerably inhibited. All these suppressive effects exhibited concentration-dependant behaviors. Pretreatment by isohamnetin (10-7 μmol/L,10-6 μmol/L and 10-5 μmol/L) significantly (P><0.01) inhibited the ox-LDL induced LOX-1 and Caspase-3 mRNA upregulation in a concentration-dependant manner. Conclusions The results show the protective effects of isorhamnetin on endothelial cells from ox-LDL induced apoptosis. These effects may be related to the inhibition of ox-LDL induced LOX-1 and Caspase-3 mRNA upregulation and the decrease of NO release.

Abstract:Aim To observe the apoptosis in endothelial outgrowth cells (EOC) induced by asymmetric dimethylarginine (ADMA) and the relevant signal transduction pathway by detecting the activity of caspase-3. Methods EOC were isolated from umbilical cord blood and then cultured. The endothelial characteristic of the cells were identified by DiI-ac-LDL and FITC-UEA-Ⅰ double fluorescent staining. Take the 0 μmol/L ADMA group as the control group. The adherent cells were treated with different concentrations of ADMA (0,1,5,10,30 μmol/L) for 48 h,then the morphological changes of cells was observed by the laser scanning confocalmicroscope. The adherent cells were treated with different concentrations of ADMA for 48 h or with ADMA(10 μmol/L)for various periods (3,6,9 h),then caspase-3 activity was measured by Microplate Reader. The adherent cells were pretreated for 30 min with ac-DEVD-CHO (100 μmol/L)-caspase-3 specific inhibitor,then 10 μmol/L ADMA was added and incubated for 48 hours. The apoptotic rate of EOC of all the groups was measured by Annexin V-FITC and Propidium iodide(PI) double staining flow cytometry. Results Typical apoptotic morphological changes can be seen in EOC after treatment of ADMA and the apoptotic rate of EOC rised accompanying with the increase of the concentration of ADMA. The activity of caspase-3 was enhanced in a dose and time dependent manner during this process. Its specific inhibitor ac-DEVD-CHO can attenuate the apoptosis induced by ADMA. Conclusion ADMA can induce apoptosis in EOC in a dose-dependent manner. This effect may be achieved by activating the intrinsic apoptoctic pathway-caspase-3 signal transduction pathway.

Abstract:Aim To explore the effects of probucol on liver protection and PPARα expression of atherosclerosis rabbits model. Methods 16 male New Zealand white rabbits were fed with 1% cholesterol,5% lard diet for 8 weeks,and then were randomly divided into two groups:high-fat group:maintained cholesterol diet for 6 weeks; probucol group:the same cholesterol diet mixed with 0.25 g/d probucol for 6 weeks. Control group was fed with normal diet for 14 weeks. This study detected the change of serum lipid profile,atherosclerotic plaque areas of aortas,histopathology and PPARα mRNA and protein expression of the livers at the end of the study. Results After 6 weeks treatment of probucol,the levels of total cholesterol (TC),high density lipoprotein cholesterol (HDLC),and low density lipoprotein cholesterol (LDLC) were reduced significantly compared with the high-fat group (P><0.05). The atherosclerotic plaque area of aortas and the histopathology of fatty liver were ameliorated in probucol group compared with high-fat group. The PPARα mRNA and protein expressions in the fatty livers of high-fat group were downregulated compared with control group,and probucol upregulated PPARα mRNA and protein expressions. Conclusion Probucol decreased the serum cholesterol and upregulated PPARα mRNA and protein expressions,which may inhibit the formation of plaques of aorta and fatty liver in atherosclerosis rabbits model.

Abstract:Aim To investigate the effect and mechanism of losartan on atherosclerosis in rabbits. Methods 32 New Zealand rabbits were randomly divided into three groups:control group,high-cholesterol group and losartan group. The level of weights,lipids and inflammatory factors,such as interleukin-6 (IL-6) and C-reactive protein (CRP) were detected before the losartan intervention and two months after the losartan intervention respectively. The content of angiotensinⅡ(AngⅡ) was detected on later stage of the experiment. Pathological examination was performed on the ratio of intima thickness to media thickness of the iliac arteries. Results After the atherosclerosis model was set up,the serum lipids and CRP,IL-6 of rabbits in high-cholesterol group and losartan group rised significantly compared to the control group,but there was no statistical difference between two groups. After the losartan intervention,serum CRP,IL-6 were higher in high-cholesterol group and losartan group compared to the control group,but lower in losartan group. Serum lipids of rabbits in high-cholesterol group and losartan group also rised significantly compared to the control group,but there was no statistical difference between them either. The ratio of intima thickness to media thickness were higher in high-cholesterol group and losartan group compared to the control group (P><0.05),but the ratio in losartan group was lower than high-cholesterol group. Angiotensin Ⅱ was higher in high-cholesterol group and losartan group compared to the control group. But there was no statistical difference between them. Conclusion Losartan can prevent the development of atherosclerosis due to its action of inhibiting inflammation and the effect of losartan on atherosclerosis may not be related to the lipid metabolism.

Abstract:Aim To investigate the effect of arecoline on the injury of endothelium dependent relaxation induced by high glucose of isolated thoracic aorta of SD rats and explore the potential mechanism. Methods Organ baths in thoracic aortic rings of SD rats were used to investigate the effect of different concentration arecoline on the injury of endothelium dependent relaxation induced by high glucose. The levels of nitric oxide (NO) and malonaldehyde (MDA) and the activity of superoxide dismutase (SOD) in the isolated thoracic aorta rings were measured. The M receptor inhibitor atropine and nitricoxide synthase inhibitor N-nitrio-L-argine methyl ester (L-NAME) were used in the study. Results Compared with the control group,endothelium dependent relaxation induced by acetylcholine of isolated thoracic aorta of SD rats was significantly decreased in high glucose group. The injury of endothelium dependent relaxation induced by high glucose was inhibited by arecoline in concentration-dependent manner. But the effect of arecoline was abolished by atropine and L-NAME. The levels of NO and the activity of SOD were decreased and the levels of MDA was increased in the isolated thoracic aorta rings by high glucose,but the effect of high glucose was reversed by arecoline. Conclusion Arecoline prevents the injury of endothelium dependent relaxation induced by high glucose,which mechanisms may be related to activation of M receptor,increase of NO and inhibition of oxidative stress induced by arecoline.

Abstract:Aim To investigate the effects of platelet factor 4 (PF4) on the expression of Toll like receptors 2 (TLR2) in human umbilical vein endothelial cells-ECV304. Methods The effects of PF4 on the expression of TLR2 in ECV304 were determined by reverse-transcription polymerase chain reaction,Western Blotting and immunohistochemistry analysis. Results In comparison with blank group,the levels of TLR2 mRNA and protein upregulated (n=5,P><0.05) in time dependent manner in PF4 (100 μg/L) group,but it could not be inhibited by heparin. Using immunohistochemical staining and image analysis methods,the TLR2 expression in ECV304 in PF4 group was increased compared with blank group(0.060 399±0.020 998 vs 0.001 385±0.000 953,P><0.05). Conclusion PF4 promotes the expression of TLR2 mRNA and protein in human umbilical vein endothelial cells. The result of study is useful for platelet to play effect on innate immunity in chronic inflammatory such as atherosclerosis.

Abstract:Aim To investigate the electrocardiographic features and its possible mechanisms at the moment of myocardial ischaemia and reperfusion injury (IRI) in patients with acute ST segment elevation myocardial infarction (STEMI). Methods The electrocardiographic changes during reperfusion of acute STEMI by thrombolysis or percutaneous coronary intervention (PCI) were analysed. Effective data of IRI electrocardiographic pattern were explored with univariate analysis. 60 cases of acute STEMI were classified into myocardial reperfusion with IRI electrocardiographic changes group (reperfusion group A,n=39) and without IRI electrocardiographic changes group (reperfusion group B,n=21). The levels of serum reactive oxygen species (ROS),malondialdehyde (MDA),reduced glutathione (GSH),total antioxidative capacity (T-AOC) and γ-glutamylcysteine synthatase (γ-GCS ) activity were measured in control group (n=43),myocardial ischaemia group (before reperfusion therapy,n=60),reperfusion group A and reperfusion group B. Results Among the 60 cases of acute STEMI,39 patients (65.00%) with IRI arrhythmia (accelerated idioventricular rhythm 26.67%,non-paroxysmal ventricular tachycardia 10.00%,sinus bradycardia 10.00%,and atrioventricular nodol block 8.33%)as well as 28 patients (46. 67%) with IRI ST segment elevation were observed. Univariate analysis revealed that the duration from chest pain to receiving reperfusion therapy,the peak time of CK-MB ,and reperfusion time were shorter in the reperfusion group B than those in the reperfusion group A (P><0.05). The more IRI electrocardiographic changes were detected during reperfusion treated by thrombolysis than by PCI (P><0.05). The levels of serum ROS and MDA in the reperfusion group A were significantly higher,but the GSH and T-AOC were significantly lower than those in the control group,myocardial ischaemia group,and reperfusion group B (P><0.05). The γ-GCS activity in reperfusion group A was significantly higher than that in the control group and myocardial ischaemia group (P><0.05). Conclusion This study confirms the occurrence of specific electrocardiographic changes (IRI arrhythmia and ST segment elevation) at the time of reperfusion. Systemic oxygen free radicals oxidative/antioxidative imbalance occurs at the moment of reperfusion in patients with acute STEMI,which may correlate to IRI electrocardiographic changes.

Abstract:Aim The present study was aimed to analyze the associations between plasma adiponectin,hemeoxygenase-1 and severity of coronary artery lesions in patients with coronary artery disease to explore the interaction between adiponectin and hemeoxygenase-1. Methods The plasma levels of adiponectin and hemeoxygenase-1 were determined by ELISA in the coronary artery disease group including 81 patients and the control group including 35 patients. Correlations were analyzed between these two biochemistry marks and the severity of coronary artery lesions(Gensini integrals). Results Plasma levels of adiponectin and hemeoxygenase-1 of coronary artery disease group were significantly lower than that of control group(4.87±0.24 vs 13.51±0.93 mg/L,P><0.001;38.85±2.86 vs 220.00±28.11 μg/L,P><0.001). Plasma levels of adiponectin and coronary artery disease in patients with more coronary artery lesions were also significantly lower than the patients with less coronary artery lesions after classification by the number of coronary artery lesions. Adiponectin was significantly associated with coronary artery disease positively(r=0.551,P><0.001). Gensini integrals was significantly correlated with adoponectin and hemeoxygenase-1 negatively(r=-0.526,P><0.001; r=-0.451,P><0.001). Conclusion Plasma adiponectin and hemeoxygenase-1 were closely associated with each other and with the severity of coronary artery lesions in patients with coronary artery disease. There're possible regulatory interactions between adiponectin and hemeoxygenase-1.

Abstract:Aim To discuss the changes of ankle brachial index (ABI),brachial-ankle pulse wave velocity (baPWV) and high sensitive C-reactive protein (hs-CRP) in 195 patients with different risk factors of atherosclerosis,and analyse its effect in the diagnosis of coronary heart disease (CHD). Methods 195 patients with possible diagnosis or having been diagnosed as coronary heart disease (CHD) with at least a merger of atherosclerosis risk factors who were hospitalized Affiliated Hospital of Ningxia Medical University on November 2008-2009 November were selected and divided into coronary artery disease (CAD) group (150 cases) and non-CAD group (45 cases). Then according to at least one coronary stenosis ≥ 50%,CAD group was divided into ≥50% group (97 cases) and <50% group (53 cases). The atherosclerosis risk factors were recorded and ABI,baPWV,hs-CRP of serum were measured. 39 healthy cases were chosen as control. Results In CAD group,non-CAD group and control group ABI had no significant difference (P>0.05),baPWV had statistically significant difference (P><0.01) and there were significant differences between the ≥50% group and <50% group (P><0.01). In non-CAD group and control group hs-CRP had no significant difference (P>0.05). However,in CAD group hs-CRP levels were significantly higher than the other two groups,there were significant differences between the two groups (P><0.01),the level of hs-CRP showed no significant difference between the two subgroups of CAD group (P>0.05). With coronary angiography as the gold standard for drawing ROC curve,ABI had no significant predictive value for CAD. CHD with higher baPWV had the predictive value with the cut-off point of 1700 cm/s,hs-CRP had a moderate predictive value with its cut-off point of 0.67 mg/L. For the combination of baPWV and CRP,the sensitivity rate was 98.0%,the specific rate was 95.8%,misdiagnosis rate was 4.2%,miss rate was 2.0%,positive predicatire value was 99% and negative predicative value was 92%,which had higher diagnostic value. Conclusions ABI and CHD was not related. baPWV increases with the extent of CHD,which had higher predictive value for CHD. hs-CRP had moderate predictive value for CHD.

Abstract:Aim To investigate the correlation between serum leptin level and intima-media thickness of carotid artery in chronic kidney disease patients (CKD). Methods Seventy-nine non-dialytic CKD patients and fifteen healthy volunteers were involved in the study. CKD patients were classified into three groups according to glomerular filtration rate (GFR):CKD 2～3 stage,CKD 4 stage and CKD 5 stage,the serum leptin was tested by the radio-immunity method; Intima-medial thickness (IMT) of carotid artery and the presence of atherosclerotic plaques were determined by using noninvasive high-resolution B-mode ultrasonography. Results Sermu leptin,IMT and prevalence of atherosclerotic plaques in CKD patients were significantly higher than those in healthy groups (P><0.01). The serum leptin and CRP concentrations were significantly increased in CKD patients with atherosclerosis of carotid artery group (17.06±1.06 ng/L vs 14.27±0.70 ng/L;P><0.05),(3.32±0.19 mg/L vs 2.55±0.17 mg/L;P><0.01). The linear correlation analysis indicated the serum leptin was correlated positively with urea nitrogen,serum creatinine,C-reaction and body mass index (r=0.293,P><0.01,r=0.324,P><0.01;r=0.539,P><0.01;r=0.312,P><0.05). The serum leptin level was correlated negatively with glomerular filtration rate,hemoglobin and albumin (r=-0.389,P><0.01;r=-0.454,P><0.01;r=-0.246,P><0.05). Logistic regression analysis further indicated that Leptin (β=1.527,P><0.05) was an independent risk factor of atherosclerosis in non-dialytic CKD patients. Conclusion The patients of CKD exist hyperleptinemia. The serum leptin was significantly correlated with IMT. Hyperleptinemia was an independent risk factor and might play a role in pathogenesis and progression of atherosclerosis.

Abstract:Aim To observe ghrelin level variation of metabolic syndrome patient and the relationship with inflammatory factor. Methods According the definition of 2005 international diabetes mellitus association,the people were divided into metabolic syndrome (MS) group and control group. RIA method was used to measure ghrelin,and ELISA method was applied to measure inflammatory factor level. The different ghrelin level of the two groups was compared,and the relationship of ghrelin and endothelial relaxation function and inflammatory level were analyzed. Results The ghrelin levels of MS group were lower than that of control group(P><0.001). The endothelial relaxation function of 1st quartile ghrelin was lower than that of 4 th quartile ghrelin; the inflammatory factor TNF-α,IL-8,MCP-1 concentrations of 1st quartile ghrelin were higher than those of 4 th quartile; correlation analysis demonstrated that ghrelin level were positively related with endothelial relaxation function,and negatively related with the inflammatory functions; multiple regression analysis suggested that the most influence ghrelin level was triglyceride,the next was systolic pressure,then age. Conclusions The ghrelin level of MS were decreased,and positively correlated with endothelial relaxation function,negatively correlated with inflammatory factor. Ghrelin may improve endothelial relaxation fuction,decrease inflammatory factor level,and prevent the development of MS.

Abstract:Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of tumor necrosis factor (TNF) super family. Combining with its receptor Fn14,TWEAK can participate in the process of atherosclerosis (As) through several ways,including inducing inflammation,augmenting the expression of MMP9,promoting neovascularization and so on. TWEAK is involved in coronary heart disease and its equivalent-diabetes mellitus. Statins may play a potential role in the treatment of As by reducing TWEAK-Fn14 complex in blood.

Abstract:Apolipoprotein A5 (apoA5) is a new member in the family of apolipoproteins. It is an apolipoprotein with low elasticity and high lipid affinity. In animals and human research,it has been identified as a regulator of triglyceride (TG) metabolism,but the relation between them is unclear. ApoA5 can help maintain the integrity of the droplet,affect very low density lipoprotein (VLDL)-TG serration,increase triglyceride-rich lipoproteins (TRL) clearance in plasma,as well as increase lipoprotein lipase (LPL) and hepatic lipase activity. However,further studies on its functions are needed.

Abstract:The rapid development of glycobiology and glycosylation make an advancement in medicine. The high incidence of cardiovascular diseases,such as atherosclerosis,hypertension,and complication caused by diabetes mellitus,seriously influenced the quality of people's life. Glycosyltransferase plays an important role in it. In recent years,people develop many new clinical drugs in application of glycosyltransferase. The study of glycosyltransferase and glucoprotein is being a new front edge of life science,which will be of great benefit for human. This article discusses the advance of glycosyltransferase in atherosclerosis.

Abstract:ISR is essentially due to vascular smooth muscle cell (VSMC) proliferation and migration,and excessive extracellular matrix production,leading to neointima formation. Rho-kinase,a major regulator of VSMC proliferation and migration,after stenting plays its role in the neointimal formation.Long-term inhibition of Rho-kinase suppresses in-stent neointimal formation by multiple mechanisms. Inhibition of the Rho/Rho kinase pathway should provide a useful strategy to prevent ISR.