Abstract:Aim To study the role of dendritic cells (DC) with lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) high expression in atherosclerosis in vitro and in vivo. Methods Western blot was used to examine the protein expression levels of LOX-1 in ox-LDL stimulated primary cultured bone marrow derived dendritic cells (BMDC) from C57 mice, flow cytometry was used to measure the ratio of LOX-1 high expression subsets and LOX-1 low expression subsets in BMDC, MACS was used to sort the two cell subsets with different LOX-1 expression and to observe the effects of ox-LDL on the ratio of two cell subsets and release of inflammatory factors. Results There were two different subsets of DC with high and low expression of LOX-1, the ratio of LOX-1^high DC was increased after ox-LDL treatment. After the LOX-1^high DC was stimulated by ox-LDL, the TNF-α and IL-1β mRNA was up-regulated (P<0.01), and the percentage of positive cells increased higher than that of negative cells. In hyperlipidemia model of C57 mice, total cholesterol levels were significantly increased after fed with high fat diet for 4,6 and 8 weeks. This was paralleled with an increase in DC number and in the ratio of LOX-1^high DC and LOX-1^low DC in the aorta from mice. Different concentrations of Dil-ox-LDL was used to stimulate DC2.4 cells, there was a concentration-dependent increase in the phagocytosis of Dil-ox-LDL by DC2.4 cells. Western blot showed that the LOX-1 expression in DC2.4 cells could be induced by ox-LDL at 20 mg/L and 40 mg/L. Conclusions Two DC subsets of LOX-1^high DC and LOX-1^low DC were found in the present study, and the levels of expression of inflammatory cytokines in LOX-1^high DC subsets were significantly higher than LOX-1^low DC subsets.In hyperlipidemia model of mice in vivo, the ratio of LOX-1^high DC and LOX-1^low DC was significantly increased in the aorta.In DC2.4 cells, ox-LDL could up-regulate LOX-1 expression.

Abstract:Aim The relationship between p38 mitogen activated protein(p38-MAPK) and low density lipoprotein receptor(LDLR) in high blood lipid and cerebral ischemia is not clear. This study aims to explore the problem. Methods SD rats were divided into normal diet group and high fat diet group feeding for 30 days and the middle cerebral artery occlusion(MCAO)was induced by the middle cerebral artery occlusion. Serum lipid levels were determined. Neural activity score, infarct weight of ischemic brain tissue and apoptosis, p-p38 expression, LDLR and p-p38 double staining index were determined to observe the effect of high fat diet on the extent of cerebral ischemia. Results Serum TG, TC, LDL of fat diet group were significantly higher than normal diet group. Neural activity score, infarct weight of ischemic brain tissue and apoptosis, p-p38 expression, LDLR and p-p38 expression were significantly higher than normal diet group. Conclusion p-p38 was located in the CA1 region. This experiment from LDLR receptor pathway and p38 MAPK signal pathway (and macrophage inflammatory link ) of two link annotation high blood lipids as risk factors of cerebral ischemiaessence, provides pharmacology reference for the treatment of hyperlipidemia induced by cerebral ischemia.

Abstract:Aim This study was designed to explore the characteristics of VSMCs phenotype during aging and hypertension, and how miR-143/145 were influenced. Methods Mesenteric arteries from 1-, 3-, 9-, and 16-month-old WKY and SHR were isolated, artery histology were evaluated by staining with HE. VSMCs phenotype marker including α-actin, Calponin, and OPN were measured. miR-143/145 were quantified by real-time PCR. Results VSMCs contractile marker α-actin and Calponin expression both reached the peak at 3M and then decreased, while OPN increased with age in SHR with no obvious changes in WKY. The expressions of α-actin, Calponin, and OPN showed significant differences between SHR and the age-matched WKY. miR-143/145 firstly increased with age and then decreased in both WKY and SHR, and miR-143/145 in WKY-3M was significantly higher than the age-matched SHR. Conclusion Aging and hypertension accelerate the VSMCs phenotype switching in arterioles, promoting the synthesis phenotype; miR-143/145 is inversely regulated with contractile VSMCs and could play a role during aging hypertension.

Abstract:Aim To evaluate the ability of capillary network formation of HUCB-late EPCs in vitro and in rat hind limb ischemic tissues, after transfected with rAAV-CXCR4 and rAAV-GFP. Methods HUCB-late EPCs were infected with rAAV₆-CXCR4、rAAV₆-GFP, and the expression of CXCR4 protein was detected by Western Blot analysis. In vitro,evaluate the ability of capillary network formation on Matrigel between the three groups. The mode of mouse hind limb ischemia was set up, by ligating the femoral artery and its branches. Following successful establishment,18 rats were divided into three groups randomly:blank group were intramuscularly injected with 500 μL EGM-2 at 6 hours following injury,and control group were intramuscularly injected with 500 μL EGM-2 at 6 hours following injury (contain 1×10⁶ non-gene transfected HUCB-late EPCs), and experiment group were intramuscularly injected with 500 μL EGM-2 at 6 hours following injury (contain 1×10⁶ CXCR4-gene transfected HUCB-late EPCs). After 28 days, capillary network in hind limb muscles and next to muscles were detected by HE stain assay,and CD31 expressed in neovascularization endothelial cells were detected by immune histochemistry assay,and calculate the number of CD31 positive neovascularization, and calculate the number of CD31 positive neovascularization. ResultsCompared with infected rAAV6-GFP and non-infected group, the expression of CXCR4 protein was up-regulated after infected rAAV₆-CXCR4. In vitro, there is no significance of tube area in unit area among three types of HUCB-late EPCs (P>0.05). In the mode of mouse hind limb ischemia, compared with blank group and control group, CD31 positive cells of new capillary network in experimental group increased obviously(P<0.05). Conclusion CXCR4 over-expression of HUCB- late EPCs could promote neovascularization in rat hind limb ischemic tissues.

Abstract:Aim Based on the signaling pathway of autophagosome formation to discuss the protective effect and mechanism of Tanshinone ⅡA on endothelial cell oxidative stress injury. Methods Culturing EA.hy926 cells in vitro, then randomly dividing these cells into normal group, model group, tanshinone ⅡA group, tanshinone ⅡA and model group, 3-MA group, model and 3-MA group, tanshinone ⅡA, model and 3-MA group. Using colorimetric method to test the cells’ MDA content and SOD activity of oxidative stress injury. Western blot detecting the expressions of cells’ autophagosome formation signaling pathway related protein. Results Compared with normal group, the MDA content is increased (P<0.01), the SOD activity is decreased (P<0.01), and the content of LC3-Ⅰ/LC3-Ⅱ protein is increased (P<0.01) in model group. There is no obvious change of LC3-Ⅰ/LC3-Ⅱ protein content (P＞0.05) in 3-MA group compared with normal group. Compared with model group, the MDA content is decreased (P<0.01), the SOD activity is increased (P<0.01) and the content of LC3-Ⅰ/LC3-Ⅱ protein is increased (P<0.01) in tanshinone ⅡA and model group. The MDA content is increased (P<0.01), the SOD activity is decreased (P<0.01), and the content of LC3-Ⅰ/LC3-Ⅱ protein is decreased (P<0.01) in model and 3-MA group compared with model group. Compared with tanshinone ⅡA and model group, the MDA content is increased (P<0.01), the SOD activity is decreased (P<0.01), and the content of LC3-Ⅰ/LC3-Ⅱ protein is decreased (P<0.01) in tanshinone ⅡA, model and 3-MA group. Compared with normal group, the expression of Atg3, Atg4b, Atg7 are increased significantly in model group (P<0.05 or P<0.01). Compared with model group, the expression of Atg3, Atg7 , Atg5-Atg12 are increased significantly in tanshinone ⅡA and model group (P<0.05 or P<0.01). Compared with tanshinone ⅡA and model group, the expression of Atg3, Atg7 , Atg5-Atg12 are decreased significantly in tanshinone ⅡA, model and 3-MA group (P<0.05 or P<0.01). Conclusion Tanshinone ⅡA may regulate the proteins of signaling pathway of autophagosome formation as well as the Atg12-Atg5 pathway and LC3-PE pathway of EA.hy926 cell to play its protective biological activities for EA.hy926 cells against oxidative stress damage, then prevent and treat the development of As.

Abstract:Aim To investigate the protective effects of berberine on viral myocarditis in mice; To study the effects of berberine on Toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB) and tumor necrosis factor α (TNF-α). Methods According to random number table, 40 BALB/c mice were divided into four groups:normal group, model group, low dose berberine treatment group and high dose berberin treatment group. Except the normal group, the mice of other groups were injected intraperitoneally with addicted concentric Coxsackie virus B3 to establish viral myocarditis model. Low dose berberine treatment group and high dose berberin treatment group were injected intraperitoneally with 50 mg/kg and 100 mg/kg respectively. The pathological changes of myocardial tissue were observed by HE staining. The serum levels of creatine kinase isoenzyme MB (CK-MB), cardiac troponin T (cTnT) and TNF-α were determined by enzyme-linked immunosorbent assay kits. Western blot and real-time fluorescence quantitative PCR were used to detect the protein expression and mRNA expression of TLR4 and NF-κB in cardiac tissue. Results Compared with the model group, inflammatory cell infiltration and cell necrosis degree in myocardial tissues were significantly decreased, and the serum levels of CK-MB, cTnT and TNF-α were significantly reduced in the berberine treatment group. At the same time, the protein expression and mRNA expression of TLR4 and NF-κB were significantly down-regulated in myocardial tissue in the berberine treatment group. Conclusion Berberine can regulate the TLR4/NF-κB signal pathway, so as to protect the myocardial tissue of mice with viral myocarditis.

Abstract:Aim To investigate the influence of homocysteine (Hcy) on CD147 expression in human U-937 macrophages and intervention effect of rosuvastatin. Methods Human U-937 macrophages induced by PMA were treated with 0,0, 100 and 500 μmol/L Hcy for 48 hours respectively, CD147 expression was then analyzed using Western blot and RT-PCR. Different concentrations of rosuvastatin (10-8~10-5 mol/L) were added when U-937 macrophages were treated with 500 μmol/L Hcy. CD147 expression was then examined after incubating for 48 h. Cellular immumofluorescence method was used to detect the expression of CD147. Results Hcy significantly increased the expression of CD147 in a dose-dependent manner. Rosuvastatin (10-7~10-5 mol/L) significantly reversed the expression of Hcy-induced CD147 in U-937 macrophages in a dose-dependent manner. Cellular immumofluorescence demonstrated that the CD147 expression of U-937 macrophages was significantly increased by Hcy compared with control group, rosuvastatin (10-5 mol/L) cloud reverse the effect. Conclusion Hcy (100~500 μmol/L) significantly increased the production of CD147 in PMA-induced U-937 macrophages in a dose-dependent manner. Additional extracellular rosuvastatin can decrease the expression of CD147 in PMA-induced U-937 macrophages induced by Hcy.

Abstract:Aim To explore the serum non-high density lipoprotein cholesterol (non-HDLC) level in patients with depression and analyze the related factors. Methods 150 depression patients were tested in Affiliated Kailuan Mental Health Center, North China University of Science and Technology from June 2014 to November 2015, testing the total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), and measuring the depressive symptoms through the self-rating depression scale (SDS). Using SPSS 17.0 software, the data was tested by independent sample t test, single factor variance analysis, partial correlation analysis and stepwise multiple regression analysis. Results There was statistical significance about differences between depression and healthy people on the serum non-HDLC level (P＜0.05). There was statistical significance about the differences on the serum non-HDLC level of depression in different gender, age, education level and depression severity (P＜0.05). After controlling the gender, age and education level, the standard score of SDS in depression had a significantly negative correlation with the TC, TG, LDLC and non-HDLC level (P＜0.05). The standard score of SDS in depression had significantly negative predictive power on the non-HDLC level (β＝－0.682, P＜0.05). Conclusion Depression is related to the non-HDLC level, and the risk and mechanism of cardiovascular disease in patients with depressive disorder should be paid attention to.

Abstract:Aim To observe the changes of serum high sensitivity C-reactive protein (hs-CRP) and endothelial cell-specific molecule-1 (ESM-1) levels and short-term prognosis of ticagrelor in treatment of patients with acute ST-segment elevation myocardial infarction (STEMI). Methods A total of 107 patients with acute STEMI were selected, all of whom were treated in department of cardiology in our hospital for new onset of symptoms and received emergency PCI successfully. The patients were divided into two groups according to the application of ticagrelor in dual antiplatelet therapy (DAPT):ticagrelor group (n=54) and clopidogrel group (n=53). Two groups of patients were observed for changes of hs-CRP and ESM-1 immediately after admission as well as 24 h, 4 d and 7 d after medication, their correlation, and influences of ticagrelor on short-term prognosis of patients with acute STEMI. Results Hs-CRP and ESM-1 of the two groups of patients were obviously elevated at 24 h after medication, and there were statistical differences (P＜0.05), and hs-CRP and ESM-1 of the two groups of patients were decreasing at 4 d and 7 d, with statistically significant differences (P＜0.05); ESM-1 was increased with the increase of hs-CRP, showing a positive correlation between ESM-1 and hs-CRP (r=0.535, P＜0.001), there were no statistical differences in comparison between the two groups in incidences of ischemic end event, hemorrhagic event and total adverse events (P＞0.05). Conclusions Ticagrelor can more quickly reduce the cell inflammation and stabilize endothelium in treatment of STEMI patients, so as to improve the stability of atherosclerotic plaque, reduce the formation of thrombus and ischemic end events, but it does not increase the risk of bleeding, which is worth of clinical application.

Abstract:Aim To investigate the clinical significance of serum growth differentiation factor 15 (GDF-15), N-terminal pro-B-type natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI) changes at different time and its relationship with short-term prognosis in patients with cardiac arrest cardiopulmonary resuscitation. Methods The serum levels of GDF-15 were detected in 102 CPR patients at instant time, 12 h, 24-48 h after CPR. According to the rise time of serum GDF-15, the patients were divided into 3 groups:(1)A group:at instant time, 12 h, 24-48 h after CPR, GDF-15 levels had been less than 1200 ng/L; (2)B group:at 12 h and 24-48 h after CPR, GDF-15 levels were increased, and more than 1200 ng/L; (3)C group:at instant time, 12 h after CPR, GDF-15 levels were increased, but GDF-15 level at 24-48 h was lower than that at 12 h. At each time point, the serum levels of NT-proBNP and cTnI, left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) were detected at the same time in 3 groups. The death situation of 3 groups was followed up for 6 months after CPR. Results GDF-15 had an interaction with NT-proBNP and cTnI (P＝0.001). LVEDD and LVEF were changed with the changes of GDF-15, NT-proBNP and cTnI levels. The mortality rates of patients in GDF-15, NT-proBNP and cTnI high level groups were higher than those in GDF-15, NT-proBNP and cTnI low level groups (P＜0.05). Survival analysis results showed that the 6 month survival rate of A group was higher than that of B group (χ²＝12.738, P＝0.001), the 6 month survival rate of B group was lower than that of C group (χ²＝7.253, P＝0.009), and there was no significant difference in 6 month survival rate between A group and C group (χ²＝2.240, P＝0.097). Conclusion The serum levels of GDF-15, NT-proBNP and cTnI are good indicators for predicting the short-term prognosis of CPR patients, and the significance of combined detection is even higher.

Abstract:Aim To explore the effect of ezetimibe on insulin release in unstable angina patients in prediabetes. Methods 222 unstable angina patients in prediabetes were randomly divided into control group and combined treatment group. In addition to routine treatment, control group was given atorvastatin 20 mg, while combined treatment group was given atorvastatin 20 mg and ezetimibe 10 mg. All patients were treated for 3 months. Oral glucose tolerance test (OGTT) and insulin release test (IRT) were examined at 7 d, 1 months, 3 months of medication. Results Compared with control group, blood glucose of OGTT on 0.5 h, 1 h, 2 h were significantly lower in combined treatment group at 7 d, 1 months, 3 months (P<0.5,0.01), and area under the curve (AUC) of blood glucose on 0.5 h, 1 h, 2 h, 3 h were significantly lower(P<0.5,0.1,0.001); insulin of IRT on 0.5 h, 1 h were significantly higher and insulin on 2 h were lower in combined treatment group at 7 d, 1 months, 3 months(P<0.5,0.01),and AUC of insulin on 0.5 h, 1 h, 2 h were significantly higher(P<0.1,0.1,0.05). AUC of blood glucose was negatively correlated with AUC of insulin (r=-0.387,P<0.01),and decrease of blood glucose was postively correlated with increase of insulin at different periods(r=0.473,P<0.001). Compared with control group, homeostasis model assessment (HOMA) for insulin resistance were significantly lower in combined treatment group at 1,3 months (P<0.5,0.01); insulin activity index at 7 d, 1 months, 3 months and HOMA-β at 3 months were significantly higher (P<0.5,0.01). Conclusion Ezetimibe can improve glucose tolerance by restored insulin release and increased insulin sensitivity on unstable angina patients in prediabetes.

Abstract:Aim To investigate the related factors of in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) in patients with coronary heart disease (CHD). Methods A total of 1342 CHD patients who received PCI in our hospital from January 2007 to January 2016 were studied. These patients were divided into ISR group (≥50% diameter stenosis of in-stent) and non-ISR group according to the result of coronary angiography (CAG). The ISR group included 89 patients (94 with lesions), and the non-ISR group included 1253 patients (1754 with lesions). Retrospective analysis of their blood biochemical index, echocardiographic index, coronary artery lesions, stents, medication compliance and major adverse cardiac events were made by multivariate models to predict the occurrence of ISR. Results The incidence of ISR was 6.6% in the selected patients. The prevalence of diabetes, smoking rate, patients with the discontinuation of clopidogrel in 1 year and discontinuation of aspirin were significantly higher in ISR group, as compared with non-ISR group (P＜0.05). Patients in ISR group taking adequate statin was more than that of non-ISR group (P＜0.05). The complex lesions, reference vessel diameter before procedure, serial stents in ISR group were higher than those in non-ISR group (P＜0.001), the stent length was longer in ISR group than that in non-ISR group (28.43±6.58 mm vs. 26.27±7.08 mm, P＝0.001), the stent diameter (2.92±0.41 mm vs. 3.04±0.43 mm, P＝0.003) and postoperative minimal lumen diameter (MLD) (2.44±0.34 mm vs. 2.57±0.35 mm, P＜0.001) were smaller and the percent of diameter stenosis (8.46% vs. 7.60%, P＝0.018) was significantly greater in ISR group than those in non-ISR group. The acute gain was lower in ISR group than that in non-ISR group (1.77±0.43 mm vs. 1.87±0.43 mm, P＝0.043). Multiariable Logistic regression analysis showed that diabetes, smoking, discontinuing aspirin, diameter or length of previously implanted drug-eluting stents (DES), postoperative MLD, serial stents, and the percent of diameter stenosis were independent risk factors for restenosis after PCI (P＜0.05). In an 8 months follow-up, the incidence of recurrent angina, target lesion revascularization (TLR) and combined major adverse cardiovascular events (MACE) in ISR group was significantly higher (P＜0.001). In the 1 year follow-up, the incidence of recurrent angina, myocardial infarction (MI), TLR, composite MACE were significantly higher in ISR group (P＜0.05). The incidence of stent thrombosis was significantly higher in ISR group (P＜0.001). Conclusions Diabetes, smoking, discontinuing aspirin, the diameter or length of previously implanted DES, serial stents, postoperative MLD and the percent of diameter stenosis are risk factors for the development of ISR. Restenosis after PCI may increase the incidence of MACE.

Abstract:Aim To assess the safety and effect of stent implantation in patients with extracranial cerebral artery stenosis in Xinjiang. Methods From 2009 to 2015, in our hospital, three hundred and twenty-three patients with symptomatic extracranial cerebral artery stenosis underwent carotid artery stenting(CAS)or vertebral artery ostium stenting (VAOS) operation. Their success rate of stent implantation,incidence of perioperative complications,and restenosis during follow-up period, modified Rankin scale(mRS)scores and events at clinical end point were compared and analyzed.Results The success rate of stent implantation in CAS and VAOS was 100％respectively,the incidence of peroperative complications was 14.4％ and 1.2％ respectively,the incidence of events at clinical end point was 15.1% and 12.8%. The incidence of restenosis was 8.8％ and 13.4％ respectively. Cox multivariate regression analysis revealed that male and multiple artery stenosis were the independent risk factors in CAS group( HR=19.249, P=0.02；HR=0.069, P=0.034), and contralateral vertebral artery stenosis was the independent risk factors in VAOS group( HR=0.075, P=0.001). Conclusion CAS and VAOS are safe and effective methods to treat extracranial cerebral artery stenosis, however, we should pay attention to the prevention and treatment of its complications.

Abstract:Aim To study the effect of urinary protein level on major adverse cardiac and cerebrovascular event (MACCE) and all-cause death in general population cohorts. Methods Prospective cohort study method was used in this study. Health examination data integrity 87292 cases were selected as the research subjects from July 2006 to October 2007 in Kailuan Group. The average age of research subjects was 51.12±12.29 years old. Urine dipstick test was used to detect morning urine. According to the level of urinary protein, population were classified into three groups:urine protein negative group (－), micro-urine protein group (±/＋), and macro-urine protein group (≥2＋). COX proportional hazards model was used to analyze the relationship between urinary protein and MACCE, all-cause death. Results The average follow-up was 6.90±0.72 years. During follow-up there were 3091 cases of MACCE, the cumulative incidence was 5.25/1000 person-year, and there were 4087 cases of all-cause death, the cumulative incidence was 6.84/1000 person-year. The cumulative incidences of MACCE in the three groups were respectively 4.84/1000 person-year, 7.34/1000 person-year, 12.06/1000 person-year. The cumulative incidences of all-cause death in the three groups were respectively 6.10/1000 person-year, 10.28/1000 person-year, 19.30/1000 person-year. The differences among the three groups were statistically significant (P＜0.01). After adjusting for other traditional risk factors, compared with urine protein negative group, RR values of MACCE in micro-urine protein group and macro-urine protein group were respectively 1.24 (95%CI 1.10-1.40) and 1.58 (95%CI 1.38-1.81), and RR values of all-cause death were respectively 1.41 (95%CI 1.27-1.56) and 2.15 (95%CI 1.93-2.39). Conclusion Urine displayed urinary protein is an independent risk factor for MACCE and all-cause death in the general population.

Abstract:Aim To investigate carotid atheroscelerotic lesions in the population ≥ 45 years of age in Dongying area. Methods Carotid artery ultrasound was performed in a total of 10 182 residents aged 45 or above. All residents were selected from 5 districts of Dongying urban and rural areas using cluster random sampling method. The carotid intima-media thickness (IMT), the plaque and vascular stenosis were recorded. Results The overall detection rate of carotid atheroscelerotic lesions was 74.8%, among which, the detection rates of simple IMT thickening, plaque formation, single plaque, multiple plaques, single carotid artery involvement, multiple carotid arteries involvement, carotid artery stent (CAS) implantation, and restenosis post CAS were 20.3%, 55.9%, 20.8%, 33.5% , 21.6%, 53.1%, 0.12%, and 0.03%. The detection rates of carotid artery mild stenosis (<50%), moderate stenosis (50%~69%), severe stenosis and occlusion (70%~100%) were respectively 73.6%, 1.0%, and 0.2%. The prevalence of carotid atheroscelerotic lesions, plaque formation, multiple plaques and multiple carotid arteries involvement in urban population were higher than that in rural population(P<0.05). There were significant differences between rural and urban population in the constituent ratio of carotid artery stenosis(P<0.05). The detection rates of carotid atheroscelerotic lesions, simple IMT thickening, plaque formation, multiple plaques, multiple carotid arteries involvement, and CAS implantation were higher in males than in females(P<0.05). Conclusion The incidence of carotid atherosclerosis in the population of Dongying area is high, the detection rate of the urban population is higher than that in rural population.

Abstract:In recent years, nonalcoholic fatty liver disease has gradually become the main factor of liver-related mortality in China. The pathogenesis of nonalcoholic fatty liver disease mainly associates with the metabolic syndrome and its risk factors include obesity, type 2 diabetes, abnormal lipid metabolism, etc. These risk factors are closely related to the cardiovascular disease. Therefore, the cardiovascular mortality has become a primary cause of death in nonalcoholic fatty liver disease. Statins are the main lipid-lowering drugs. There is evidence that nonalcoholic fatty liver disease patients using statins not only can effectively reduce the liver transaminase level and the mortality of cardiovascular disease, but also can effectively improve hepatic steatosis, and may delay progression of liver fibrosis.

Abstract:Recently, a new class of antidiabetic drugs, dipeptidyl peptidase-IV (DPP-4) inhibitors, has gained considerable interest in different fields. In addition to lower glucose and improve insulin resistance, DPP-4 inhibitors have exhibited pleiotropic effects, including cardioprotection, angiogenesis, hematopoiesis recovery and inflammation inhibition via the regulation of the substrates, such as glucagon-likepeptide-1 (GLP-1), stromal cell-derived factor-1α (SDF-1α), vascular endothelial growth factor (VEGF) and high mobility group box 1 (HMGB1) etc. The role of DPP-4 in cardiovascular disease has been fully reported by previous studies, so the goal of this review is focused on the function and mechanism of DPP-4 and its inhibitors in vascular regeneration, and developing a better understanding of the drugs.

Abstract:High density lipoprotein-cholesterol (HDLC) is regarded as an important protective factor against cardiovascular disease. There is an inverse relationship between its serum levels and risk of cardiovascular disease. However, in cardiovascular disease, diverse components of the high density lipoprotein(HDL) proteins,lipids or microRNAs suffer alterations, which propel a shift towards a dysfunctional state, where HDL becomes proatherogenic, prooxidant, and proinflammatory. This review is to summarize the structural and functional changes of the dysfunctional high density lipoprotein.

Abstract:With the accelerated aging of society, the incidence of atherosclerosis(As) is increasing year by year. Now that the initial event of the atherosclerosis is endothelial damage, while lipid metabolism is a major risk factor for vascular injury. But now research shows that some non-lipid material also play an important role in the development of As, such as high homocysteine (HHCy), high blood sugar and high uric acid. These non-lipid factors play a major role in vascular endothelial cells, interference by expression of sticky molecule, changing the state of the pathophysiology of endothelial cells, leading to endothelial damage, contributing to the formation of As lesions. This paper describes some of the mechanisms that the changes of adhesion molecules in non-lipid factors induced atherosclerotic vascular endothelial injury, and describes some of the therapeutic intervention targets expression of adhesion molecules, which has important clinical significance for the treatment of atherosclerosis leading to coronary heart disease, myocardial infarction and other cardiovascular diseases.

Abstract:Autophagy is a highly conserved catabolisml process of self-degradation responsible for maintaining cellular homeostasis. Vascular calcification is common in many diseases such as atherosclerosis, diabetes and end-stage renal disease,which is a major risk factor of cardiovascular mortality. Today the effective therapy for vascular calcification is still unavailable. Recent studies indicate that vascular smooth muscle cells (VSMCs) autophagy may play an important role in vascular calcification by regulating the activity of self-degradation and the transdifferentiation process of VSMCs to osteogenic phenotype. This article briefly reviews the recent advances between VSMCs autophagy and vascular calcification.