Abstract:Aim To investigate the mechanism of high sodium salt induced proliferation of cardiac fibroblasts (CFs) and the intervention effect of dendrobine. Methods Rat CFs were cultured with tissue explant method in vitro.The experiments were divided into 3 groups:control group (containing 139 mmol/L Na＋), high sodium salt group (containing 161 mmol/L Na＋), dendrobine group (161 mmol/L Na＋＋10－5 mol/L dendrobine), and cells were cultured for 48 hours. CCK-8 cell proliferation kit and MTT colorimetric assay were used to detect the proliferation of cells in each group.The protein expressions of proliferating cell nuclear antigen (PCNA), phosphorylated extracellular regulated protein kinase 1/2 (p-ERK1/2) and phosphorylated nuclear factor κB p65 (p-NF-κB p65) were detected by Western blot assay. The mRNA expressions of monocyte chemotactic protein 1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were detected by real-time fluorescence quantitative PCR. Results Compared with the control group, the proliferations of CFs in the high sodium salt group were significantly increased after 48 hours culture. Compared with the high sodium salt group, 10－5 mol/L dendrobine could significantly inhibit the proliferation of CFs. Compared with the control group, the protein expressions of p-ERK1/2 and p-NF-κB p65 were increased, inflammatory factors MCP-1, VCAM-1 and ICAM-1 mRNA expressions were increased in high sodium salt group. Compared with the high sodium salt group, dendrobine could significantly reduce the expressions of PCNA and p-NF-κB p65 proteins and the expression of MCP-1 mRNA, but had no significant effect on the expressions of p-ERK1/2, VCAM-1 and ICAM-1. Conclusion High sodium salt induces the proliferation of CFs and the expression of inflammatory factors, and its mechanism is related to the upregulation of p-ERK1/2 and p-NF-κB p65 expressions. Dendrobine inhibits these effects and its mechanism is related to the inhibition of p-NF-κB p65.

Abstract:Aim To explore the effect of dasatinib on proliferation, migration, cell cycle and apoptosis of human umbilical vein endothelial cells cytologically and molecularly to offer help on clinical application of dasatinib. MethodsExperimental grouping:dasatinib group (dasatinib concentration was 50 nmol/L) and LY294002 group (PI3K inhibitor,concentration was 20 μmol/L), combined treatment group (dasatinib treatment concentration was 50 nmol/L, the concentration of LY294002 for 20 μmol/L) and mock group (DMSO was 0.1%). Cell viability was measured by CCK8. The migration ability of human umbilical vein endothelial cells was measured by scratch assay. Apoptosis and cell cycle were analyzed by flow cytometry. The expression and phosphorylation of Akt protein were determined by Western blot. Results The cell viability of human umbilical vein endothelial cells decreased gradually following the increasing concentration (1~400 nmol/L) and prolonged exposure to dasatinib (50 nmol/L, 24~96 h). Dasatinib and LY294002 (an inhibitor of PI3K), both inhibited cell viability of human umbilical vein endothelial cells. Dasatinib (50~100 nmol/L) weakened the migration capability of human umbilical vein endothelial cells. In addition, compared with control, dasatinib (50 nmol/L) induced apoptosis and cell cycle arrest (P＜0.05) of human umbilical vein endothelial cells. The phosphorylation of Akt was inhibited by dasatinib and LY294002, and LY294002 had more powerful inhibition of p-Akt than dasatinib. Conclusion Dasatinib could facilitate the injures of human umbilical vein endothelial cells via PI3K/Akt pathway, mainly to suppress the proliferation and migration of human umbilical vein endothelial cells, alter the cell morphology, blocked the G1-S transition and induced apoptosis.

Abstract:Aim To screen miRNA for efficient regulation of LPA gene expression. Methods The miRNA of LPA gene 3′UTR were predicted by on-line prediction tools. The mRNA and protein expression of apolipoprotein(a) (Apo(a)) were detected by RT-PCR and Western blot after transfection. The experiment was divided into 4 groups:control group, miR-626 mimic group, miR-626 mimic+miR-626 inhibitor group and miR-626 inhibitor group. The miR-626 target validation assay was performed using a luciferase reporter system. Results There were 9 miRNA binding 3′UTR of LPA gene. Compared with the control group, the expression of Apo(a) mRNA was not significantly different between the mimic transfected group and the control group, but miR-626 significantly down-regulated the expression of Apo(a) protein. MiR-626 attenuated Apo(a) protein down-regulation by miR-626 inhibitor. The fluorescence intensity of the miR-626 cells was significantly lower than that of the control group after cell lysis. Conclusion MiR-626 down-regulates the expression of Apo(a) in HepG2 cells. MiR-626 down-regulates the expression of Apo(a) protein in LPA mRNA by direct binding to LPA mRNA 3′UTR.

Abstract:Aim Human umbilical vein endothelial cells (HUVEC) were incubated with high homocysteine (Hcy) in vitro, establishing inflammatory damage model of vascular endothelial cell, after intervening with Diplacone, to observe the effect of Diplacone on HUVEC, and to explore the possible protective effect of Diplacone on vascular endothelial cell. Methods HUVEC were pretreated with different concentrations of Hcy, choosing the optimal damage concentration and time of Hcy. HUVEC were treated with different concentration of Diplacone for 2 hours then treated with Hcy for 12 h. The change of cell activity was detected by MTT method; Cell nucleus damage was detected by Hoechst33342 stain; Protein expression levels of vascular cell adhesion molecule-1 (VCAM-1) and P-seletin were detected by Western blot method. The above tests were used to show the protective effect of Diplacone on HUVEC induced by high Hcy. Results Compared with the normal group, the activity of the 2 mmol/L Hcy group was significantly lower (P<0.01), while Diplacone concentration was less than 10 μmol/L, Diplacone showed a concentration dependent on decreasing the damage of Hcy on HUVEC and decreased VCAM-1 and P-selectin protein expression that were increased by Hcy in HUVEC (P<0.01). Conclusion Diplacone has protective effect on endothelial injury induced by high Hcy in HUVEC.

Abstract:Aim To investigate whether there is a difference between HDLPCHD and HDL_health against human umbilical vein endothelial cells apoptosis in patients with premature coronary heart disease (PCHD) and the possible mechanism. Methods Blood samples of PCHD patients and healthy subjects were collected, and HDL was isolated from the blood samples. Human umbilical vein endothelial cells were treated for 24 hours with different concentrations of oxidized low density lipoprotein (ox-LDL), cell viability was detected by MTT, to identify the appropriate concentration of ox-LDL induced human umbilical vein endothelial cells cell apoptosis. Human umbilical vein endothelial cells were pretreated with different hours and different concentration of HDL_health, then treated with the appropriate concentration of ox-LDL for 24 hours, cell viability was detected by MTT, to identify the optimal concentration and time of HDL_health pretreated human umbilical vein endothelial cells. Human umbilical vein endothelial cells were pretreated with the optimal hours and the optimal concentration of HDL_health and HDLPCHD, then treated with the appropriate concentration of ox-LDL for 24 hours, cell viability was detected by MTT. Annexin V-FITC/PI apoptosis detection kit was used for flow cytometry staining, Western blot was used to detect Caspase 3 and Caspase 9 protein expression, kit was used to detect the activity of reactive oxygen species (ROS), sub-fraction (HDL₁-HDL₁₀) distribution of HDL_health and HDLPCHD were analyzed by Lipoprint System. Results Human umbilical vein endothelial cell survival rate was 60.34% after treatmented with 100 mg/L ox-LDL for 24 hours, which was significantly lower than that in the blank treatment group (P＜0.05). Human umbilical vein endothelial cell survival rate was 82.01% after pretreated with 200 mg/L HDL_health for 18 hours, which could significantly reduce the damage of ox-LDL to cells. 200 mg/L HDL_health could significantly inhibit apoptosis of human umbilical vein endothelial cells, the expression of Caspase 3 and Caspase 9 and the production of ROS , which were induced by 100 mg/L ox-LDL. Human umbilical vein endothelial cell survival rate was 65.5% after pretreated with 200 mg/L HDLPCHD for 18 hours, and its effect was weaker than that of HDL_health. 200 mg/L HDLPCHD could inhibit apoptosis of human umbilical vein endothelial cells, the expression of Caspase 3 and Caspase 9 and the production of ROS induced by 100 mg/L ox-LDL, but the effect was weaker than that of HDL_health. The content of large particle (HDL₁-HDL₃) in HDLPCHD subgroup was lower than that in HDL_health (28.5%±5.7% vs. 46.8%±15.2%), while the content of small particle (HDL₈-HDL₁₀) was higher than that of HDL_health (21.4%±7.8% vs. 10.9%±5.4%). Conclusion Comparison to the HDL_health, perhaps due to the large particle of HDLPCHD sub-fraction content (HDL₁-HDL₃) was lower than that of HDL_health, while the small particle was higher than that of HDL_health (HDL₈-HDL₁₀), resulting in antioxidant function weakened, inhibiting the apoptosis of endothelial cells induced by ox-LDL were decreased, thereby weakening or losing the role of anti-atherosclerosis.

Abstract:Aim To explore the effect of aerobic exercise on endothelial function in elderly spontaneously hypertensive rats (SHR), and the oxidative stress mechanism. Methods Sixteen-month-old male spontaneously hypertensive rats (n＝24) and male Wistar Kyoto rats (WKY, n＝24) with the same age were selected. Wistar Kyoto rats and spontaneously hypertensive rats were randomly assigned to sedentary control groups (WKY-C and SHR-C) and exercise-trained groups (WKY-EX and SHR-EX), seperately. The animals in exercise-trained groups ran on a motor treadmill (0° slope, 5 d/w, 60 min/d) at 16~18 m/min for 8 weeks. Blood pressure was examined by non-invasive methods, isolated vessel rings were applied to evaluate vasomotor response, plasma samples were used for measurement of NO level and relative oxidative stress markers. Results The systolic blood pressure was significantly lower in SHR-EX group than that in SHR-C group (P＜0.05). Serum malondialdehyde (MDA) in SHR-EX group (7.9±0.3 μmol/L) was lower than that in SHR-C group (11.8±1.0 μmol/L, P＜0.05), serum MDA in SHR-C group was significantly higher than that in WKY-C group (7.2±0.3 μmol/L, P＜0.05). Antioxidant enzymes including glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD), however, there was no significant difference between four groups. Exercise had significant changes of NE-induced vascular contraction in SHR (SHR-EX:136.0±1.8 %KMAX; SHR-C:153.2±1.9 %KMAX, P＜0.05). Compared with SHR-C group, NE-induced vascular constriction in WKY-C group (120.2±5.6 %KMAX, P＜0.05) were significantly lower, and that in WKY-EX group (143.9±4.3 %KMAX) were significantly higher than that in WKY-C group (P＜0.05). Endothelium-dependent vasodilaton in SHR-C group (50.2±2.8 %NE) was significantly lower than that in WKY-C group (100.1±0.6 %NE, P＜0.05), endothelium-dependent vasodilaton in SHR-EX group (97.0±1.5 %NE) was significantly higher than that in SHR-C group (P＜0.05). After 15 min incubation with NADPH oxidase inhibitor Apocynin in vitro, endothelium-dependent vasodilaton in SHR-C group (98.6±1.3 %NE) significantly increased. NO-dependent vasodilation in SHR-C group (25.5%±2.3%) was significantly lower than that in WKY-C group (85.2%±0.7%, P＜0.01), NO-dependent vasodilation in SHR-EX (86.8±3.4%) and WKY-EX(98.8±1.5%) was significantly higher than the corresponding control group (P＜0.05). Conclusion Long-term aerobic exercise inhibits the increase of oxidative stress and the decrease of NO bioavailability induced by aging and/or hypertension and improves vascular endothelial dysfunction.

Abstract:Aim To investigate the effect and mechanism of Klotho on lipopolysaccharide(LPS) induced cardiomyocyte damage. Methods H9c2 cells were pretreated with different concentrations of Klotho protein, then treated with 1 g/L LPS for 6 hours, and cardiomyocyte damage was estimated by detecting the content of lactate dehydrogenase(LDH) and cell viability. Inflammation was estimated by detecting the content of tumor necrosis factor-α (TNF-α), interleukin-β(IL-β), IL-6. The status of oxidative stress was measured by malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px). Cell apoptosis was measured with flow cytometry. The expression of nuclear factor-κB (NF-κB)p65 and p-NF-κB p65 at protein levels were measured with Western blot assay. Results Klotho can alleviate LPS-induced decrease of cell viability, inhibit the release of LDH, TNF-α, IL-β, IL-6, down-regulate the content of MDA, enhance the activity of SOD, GSH-Px, suppress cell apoptosis and p-NF-κB p65 protein expression (P<0.05). Conclusion Klotho can alleviate LPS-induced cardiomyocyte damage. And its mechanism may be related to the downregulation of NF-κB activation, and protect H9c2 cells from LPS-induced inflammation, oxidative stress and cell apoptosis.

Abstract:Aim To explore the effect of Baicalin on blood pressure and left ventricular remodeling in rats with renal hypertension. Methods Amogn 40 male Wistar rats 10 were randomly selected for sham operation group, which renal hypertensive rat model was established by using two kidney one clip method. The rats with renal hypertension were randomly divided into model group and Baicalin group after 6 weeks, eventually alive rats were devided into sham operation group (n=9), model group (n=10) and Baicalin group (n=11) for 4 weeks intervention. During the experiment, the general situation of rats was observed, and the blood pressure were detected before operation, operation after 6 weeks, and intervention for 4 weeks; high frequency echocardiography were detected after 4 weeks and the cardiac function indexes were measured. The rats were sacrificed and the heart was removed. The morphological changes of myocardial tissue was observed by using HE staining, Masson staining. The myocardial apoptosis was detected by TUNEL method and the expression of endoplasmic reticulum chaperone glucose regulated protein(GRP78), glucose regulated protein(GRP94) in myocardial cell of rats were also detected by real-time PCR and Western blot. The expression of CCAAT/enhancer binding protein homologous protein(CHOP) and Caspase 3 was monitored by Western blot. Results Compared with model group, there was significant change of blood pressure in Baicalin group (P<0.05), and the indexes of left ventricular remodeling were significantly improved after the echocardiography(P<0.05). Compared with model group, the integral of pathological myocardial fibrosis and fibrosis related factors matrix metalloprotein-9(MMP-9), matrix metalloprotein-2(MMP-2), connective tissue growth factor(CTGF) and transforming growth factor-β1(TGF-β1) expression was significantly decreased in Baicalin group(P<0.05). Compared with model group, the expression of GRP78, GRP94, CHOP, Caspase 3 and apoptosis of cardiomyocyte were significantly decreased in Baicalin group(P<0.05). Conclusion Baicalin had a certain antihypertensive effect, it could improve the left ventricular remodeling in renal hypertensive rats, reduce myocardial pathological changes, ease the endoplasmic reticulum stress and reduce apoptosis in myocardial cell.

Abstract:Aim To investigate the association between apolipoprotein (ApoM) gene and coronary heart disease (CHD) by detecting the polymorphism of ApoM rs707921 site. Methods The polymorphism of ApoM rs707921 site was detected by single fluorescent labeling probe technique in 111 cases of CHD patients and 248 cases of control group. The distribution of genotype and allele frequency was analyzed. Results The frequencies of ApoM rs707921 genotype (AA, AC and CC) were 1.8%, 13.5% and 84.7% in CHD group, 2.0%, 25.4% and 72.6% in control group, respectively, there was significant difference between the two groups (P＝0.039). The frequencies of A and C allele in ApoM rs707921 site were 8.6% and 91.4% in CHD group, 14.7% and 85.3% in control group, respectively, the difference between the two groups was statistically significant (P＝0.023). Triglyceride level of AC＋AA genotype was significantly lower than that of CC genotype in CHD group (P＝0.043). There was no significant difference in the severity of coronary artery lesion between different genotypes of rs707921 polymorphism in CHD group (P＞0.05). Conclusion A allele of ApoM gene rs707921 site may reduce the risk of CHD, but has nothing to do with the severity of coronary heart disease.

Abstract:Aim To investigate the relationship between acute ischemic stroke (AIS) and miR-335 gene(MIR335) promoter methylation of peripheral blood leucocyte in patients. Methods The study included 30 AIS patients and 30 age- and sex-comparable healthy controls. Bioinformatics database analysis was used to describe the CpG island of MIR335 promoter region. The quantitative methylation level in the 33 CpG sites of the MIR335 promoter was measured by bisulfite sequencing PCR in each participant. Stroke severity was evaluated by the National Institutes of Health Stroke Scale (NIHSS). Results Bioinformatic searches show that the fragment surrounding the transcription start site of MIR335/MEST exhibits a characteristic CpG island which overlaps with the promoter region. Compared with healthy controls, the levels of MIR335 promoter methylation were significantly higher in stroke patients (P<0.01). The level of MIR335 promoter methylation was negatively correlated to the level of plasma miR-335(r=－0.72,P<0.01), and positively correlated to NIHSS (r=0.74, P<0.01). Conclusion Ischemic stroke patients have higher MIR335 promoter methylation levels in the peripheral blood leucocyte than those in the controls. The study implies that hypermethylation of MIR335 promoter CpG island might be involved in ischemic stroke.

Abstract:Aim To explore the serum levels of interleukin-1 (IL-1) and interleukin-6 (IL-6) in patients with chronic heart failure accompanied with renal damage and its clinical significance. Methods 220 New York Heart Association (NYHA) functional class Ⅱ~Ⅳ patients with chronic heart failure were enrolled in this study. Serum levels of blood urea nitrogen (BUN), serum creatinine (SCr), N-terminal pro-B-type natriuretic peptide(NT-proBNP), IL-1 and IL-6 were detected, microalbuminuria (MAU) was detected randomly, left ventricular ejection fraction (LVEF) was measured by echocardiography, glomerular filtration rate (eGFR) was calculated. The levels of IL-1, IL-6, NT-proBNP, MAU and eGFR in different cardiac function groups were compared and the levels of IL-1 and IL-6 in different renal function groups were compared. The relationship between IL-1, IL-6 and NYHA functional classification, NT-proBNP, LVEF, eGFR and MAU were analysed. Results The serum levels of IL-1, IL-6, NT-proBNP and MAU in NYHAⅢ～Ⅳ groups were higher than NYHA Ⅱgroup (P＜0.05), the eGFR of NYHAⅢ～Ⅳ groups were lower than NYHA Ⅱgroup (P＜0.05), and the levels of IL-1, IL-6, NT-proBNP and MAU in NYHA Ⅳ group were higher than NYHA Ⅲ group (P＜0.05). In NYHA functional class Ⅲ～Ⅳ patients the serum levels of IL-1, IL-6, NT-proBNP and MAU in 30%≤EF≤50% group were higher than EF＞50%group (P＜0.05), the eGFR of 30%≤EF≤50% group were lower than EF＞50% group (P＜0.05), the serum levels of IL-1, IL-6, NT-proBNP and MAU in EF＜30% group were higher than 30%≤EF≤50% group (P＜0.05). In NYHA functional class Ⅲ～Ⅳpatients the serum levels of IL-1, IL-6 in renal dysfunction group [eGFR＜60 mL/(min.1.73m²)] were higher than normal renal function group [eGFR≥60 mL/(min.1.73m²)](P＜0.05). The serum levels of IL-1, IL-6 and eGFR had no obvious difference in different basic etiologies groups (P＞0.05). The serum levels of IL-1 and IL-6 were positively correlated with the NYHA functional classification, MAU and NT-proBNP (P＜0.05), negatively correlated with LVEF and eGFR (P＜0.05). Conclusion The serum levels of IL-1 and IL-6 are elevated in patients with chronic heart failure and correlated with the severity of chronic heart failure and renal damage, and detecting IL-1, IL-6 may provide some assistances for assessing the severity of heart failure in clinical.

Abstract:Aim To explore the relationship between soluble growth stimulation expressed gene 2 (sST2) and myocardial fibrosis after acute myocardial infarction (AMI). Methods 249 cases were selected from January 2015 to September 2016 in the First Hospital of Lanzhou University, AMI group had 166 cases that were first diagnosed as AMI patients, while 83 cases of coronary angiography negative in the control group. The level of serum sST2, procollagen Ⅲ N-terminal peptide (PIIINP), aminoterminal pro-brain natriuretic peptide (NT-proBNP) were tested and left ventricular ejection fraction (LVEF), left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) were collected, compared and analyzed. Results Serum sST2, PⅢNP and NT-proBNP levels and values of LVESV and LVEDV in AMI group were higher than those in control group, values of LVEF in AMI group were lower than those in control group (P＜0.05 or P＜0.01). Serum sST2 level in LVEF＜50% subgroup of AMI group was higher than LVEF≥50% subgroup (P＝0.031). Serum levels of sST2 were positively correlated with PⅢNP (r＝0.181, P＝0.02), and negatively correlated with LVEF (r＝－0.179, P＝0.021) in group AMI. Serum sST2, NT-proBNP and sST2＋NT-proBNP in AMI group could diagnose heart failure after AMI, and their areas under ROC curve were 0.8,0.683 and 0.732 respectively. Conclusion Serum sST2 participates in the process of myocardial fibrosis after AMI, and is correlated with left ventricular systolic function. Serum sST2 levels have diagnostic value in heart faliure after AMI.

Abstract:Aim To observe the effect of Xingling dispersible tablets on carotid atherosclerotic plaque, inflammatory factors and National Institutes of Health Stroke Scale (NIHSS) in patients with cerebral infarction, and to explore its therapeutic value. Methods 98 patients with cerebral infarction with carotid atherosclerotic plaque were randomly divided into control group and treatment group. On the basis of the control group, the treatment group was treated with Xingling dispersible tablets for 3 months. NIHSS, carotid atherosclerotic plaque area and carotid intima-media thickness (IMT) were observed before and after treatment, and the changes of serum C-reactive protein (CRP), homocysteine (Hcy) and interleukin-1β (IL-1β) were also measured. Results There was no significant difference before treatment in the NIHSS score, plaque area and IMT between the treatment group and the control group (P>0.05), but significantly decreased after treatment (P<0.001). After treatment, the NIHSS score, plaque area and IMT were lower in the treatment group than those in the control group (P<0.001). There was no significant difference in the levels of CRP, Hcy and IL-1β between the two groups before treatment (P>0.05), but significantly decreased after treatment (P<0.001). After treatment, CRP, Hcy and IL-1β in the treatment group were lower than those in the control group (P<0.001) . Conclusion Xingling dispersible tablets may inhibit the inflammation and delay the progress of carotid atherosclerosis, so as to improve the neurological deficit.

Abstract:Aim To investigate the clinical and imaging characteristics of moyamoya disease complicated with coronary artery stenosis. Methods The clinical manifestations, imaging characteristics and prognosis of 8 patients with moyamoya disease complicated with coronary artery stenosis were analyzed. Results 8 cases of moyamoya disease were acute onset, including 6 cases of cerebral infarction and 2 cases of cerebral hemorrhage. Among them, 3 cases underwent coronary artery stent implantation. 8 cases were improved and discharged, and followed up for a period of 3 months, 1 case died of recurrent cerebral hemorrhage, and the other patients had different degrees of sequelae. Conclusion Moyamoya disease combined with coronary artery stenosis is extremely rare, and vascular lesions of moyamoya disease may not only involve the cerebral vessels.

Abstract:Aim To prepare the no-reflow model after myocardial ischemia-reperfusion injury in rats and to explore the key points in the establishment of the model, so as to provide reference for the successful replication of the disease model. Methods Twenty SD rats were randomly divided into no-reflow group (n＝15) and sham group (n＝5). In the no-reflow group, the left anterior descending artery (LAD) was ligated 45 min and then perfused 120 min. The sham group rats underwent the same surgical procedures except that LAD was not ligated. At the end of reperfusion, thioflavin S staining was performed to determine the area of no-reflow (ANR), while monitoring the changes of respiration and electrocardiogram (ECG) in rats. Results Twenty rats were all survived, at the selected condition of ischemia and reperfusion time, all the rats in the no-reflow group showed obviously myocardial no-reflow phenomenon. After no-reflow model was established, the heart rate accelerated and ST segment elevation increased in the ischemic stage. Along with a progress of reperfusion, the heart rate and amplitude increased first and then decreased, while the increase values of ST segment drop less than 30%. Conclusion The method can successfully replicate the animal model of no-reflow and the method has high success rate and high animal survival rate.

Abstract:It has been widely accepted that atherosclerosis is a chronic inflammatory disease of blood vessels, and immune cells play an important role in atherosclerosis, but the specific mechanism of the inflammatory immune factors still need more comprehensive and in-depth discussion. With the development of technology,the importance of glycobiology in immune response has been found. Among them, sialic acid binding immunoglobulin-like lectin (Siglec) families is closely related to inflammatory immune cells and have higher species-specific. Siglec-1,5 and 7 are associated with the activity of monocyte and macrophage, Siglec-2 and 10 modulate the activity of B lymphocyte, Siglec-5,9 and 14 are associated with the activity of neutrophil. It is indicated that Siglec may take part in the formation of atherosclerosis through regulating the activity of immune cells. Although there is few direct evidence supporting the hypothesis, studies have shown that inhibition of Siglec-1 expression can attenuate atherogenesis in ApoE-deficient mice. The study tries to explore new mechanism of inflammatory immune factors in atherosclerosis and new potential targets to prevent the atherosclerosis through the perspective of glycobiology. Therefore, it discusses the advances in the relationship between Siglec and atherosclerosis associated immune cells.

Abstract:Atherosclerosis (As) disease, under the influence of various vulnerable factors, eventually leads to the formation and rupture of plaques. In this process, the quantity and permeability of plaque neovascularization are the key factors. Therefore, the regulation of angiogenesis has become a therapeutic strategy for As disease in recent years. However, there are some limitations only by inhibiting the development of new blood vessels, and how to promote the maturation of vasa vasorum in the plaque will become a new way to stabilize the vulnerable plaque of As. In this paper, we review the growth factors and signaling pathways related to the maturation of vasa vasorum, in order to lay a theoretical foundation for the new treatment of vulnerable plaque in As.

Abstract:Sphingosine-1-phosphate receptors are important targets for sphingosine-1-phosphate to play roles in cells, and five subtypes of sphingosine-1-phosphate receptors are included, which are widely expressed in all systems including cardiovascular system. The receptors have various important biological effects on vasodilatation, vascular endothelial barrier function, ischemia reperfusion injury, atherosclerosis, etc. This paper makes a review on roles and mechanisms of sphingosine-1-phosphate receptor 3 in cardiovascular system.

Abstract:Ischemia reperfusion injury, an important clinical problem that is caused by interruption of blood supply to tissue followed by blood reflow into the exposed area, is commonly seen in clinic and is difficult to avoid. Klotho, an anti-aging protein, possesses a variety of functions including anti-oxidative stress, anti-apoptosis, anti-inflammation, calcium overload inhibition and so on. This review summarizes the current knowledge of the involvement of Klotho in ischemia reperfusion injury and its possible mechanisms, attempting to provide some basis for the research and development of new drugs for the treatment of ischemia reperfusion injury.

Abstract:Creatine kinase(CK) is considered related to the formation and development of hypertension as it participates in the energy transfer, regeneration and utilizing in cells. And it is gradually becoming a hot research topic in the field of high blood pressure. This paper will make a summary of the creatine kinase and hypertension correlation research progress, the possible mechanism and new drug research.