Abstract:Aim To investigated the role and mechanism of macrophage in endothelial dysfunction and cardiac hypertrophy in AngⅡ-induced hypertensive mice. Methods C57BL/6 mice were randomly divided into four groups:normal+PBS group, normal+clodronate liposome (CL) group, Ang Ⅱ+PBS group, Ang Ⅱ+CL group. PBS or CL was injected via tail vein,and Ang Ⅱ was delivered by implantation of osmotic mini-pump. The systolic blood pressure (SBP) was measured by tail-cuff method, SBP was measured at 3 time points:at baseline, 7 days and 14 days after AngⅡ infusion. HE staining was used to measure myocardial hypertrophy, endothelium dependent relaxation to acetylcholine in aortic rings was determined by organ chamber bath, the protein expression of p-eNOS, p-ERK1/2 , TNF-α, IL-1β, TGF-β1, fibronectin was determined by Western blot. Results Compared with the normal+PBS mice, AngⅡ+PBS significantly increased systolic blood pressure (44%,P<0.05), macrophage infiltration in myocardial tissue (54%, P<0.05), heart weight (29%, P<0.05) as well as single myocardial cell area (48%, P<0.05), impaired acetylcholine-induced endothelium dependent relaxation (E_max-35%, P<0.05). The treatment with CL significantly reduced SBP (-25.28%, P<0.05), the area of single myocardial cell (-38.83%, P<0.05), and improve acetylcholine-induced endothelium dependent relaxation (E_max 12.63%, P<0.05) in AngⅡ hypertensive mice. CL treatment also restored the expression of p-eNOS, p-ERK1/2, TNF-α, IL-1β, TGF-β1, fibronectin induced by AngⅡ (P<0.05). Conclusions The results demonstrate that CL protects against AngⅡ-induced endothelial dysfunction and myocardial damage and remodeling, the underlying mechanisms may involve reduction in myocardial macrophage infiltration and macrophage-derived cytokines.

Abstract:Aim To investigate the relationship between microRNA (miRNA) and autophagy in aged myocardial cells induced by D-galactose. Methods The D-galactose with 0, 4, 8, 16, 20 g/L was used to induce the rat myocardial cells to senescence respectively,and being stimulated 3,6, 9 days later, the aging level of H9c2 was detected by the beta-galactosidase staining； the formation of autophagosomes in aging rat cardiomyocytes induced by D-galactose was detected by electron microscope； the mRNA expression level of miRNA-30a, miRNA-126, miRNA-204 and protein expression level of LC3B II/LC3B I in aging rat cardiomyocytes and H9C2 cells was detected by quantitative real-time(qRT-PCR) and Western blot methods respectively. Results Compared with the control group, the cell staining was gradually deepened with the increase of drug concentration and the stimulation days, and when D-galactose concentration was 8 g/L for 9 days, cell staining was the most obvious； electron microscopy showed that the autophagy in aging cardiomyocytes induced by D-galactose was decreased； Western blot results showed that the level of LC3B II/LC3B I in aging cardiomyocytes was reduced； qRT-PCR results showed that in the aging cardiomyocytes group the expression levels of miRNA-30a and miRNA-126 were decreased and miRNA-204 was significantly increased. Conclusion In the process of the autophagy level decreasing in senescent cardiomyocytes induced by D-galactose, there exists a reducing in miRNA-30a, miRNA-126 expression level and an increasing in miRNA-204 expression level, the differential expression of miRNAs may be an important mechanism of autophagy in senescent cardiomyocytes.

Abstract:Aim To investigate the effect of high mobility group box 1 (HMGB1) and its receptor on survival and cytokine levels of rat marrow mesenchymal stem cells. Methods Marrow mesenchymal stem cells were treated with HMGB1 at 25.0,0.0 and 100.0 μg/L for 4,8 and 72 hours. Cell proliferations were detected by MTT after different treatment. VEGF and bFGF were detected by ELISA. Expressions of receptor of advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4) in mesenchymal stem cells were detected by Western blot. Real-time PCR and Western blot were used to examine RAGE and TLR4 expression, which were to verify the efficiency of transfection with siRNA in marrow mesenchymal stem cells. MTT assay and ELISA were used to analyze proliferation and secretions of VEGF and bFGF in si-RAGE or si-TLR4 marrow mesenchymal stem cells. Results 25.0 μg/L HMGB1 could increase marrow mesenchymal stem cells proliferation (P＜0.05). 25.0 and 50.0 μg/L HMGB1 could promote VEGF and bFGF secretion compared with control group (P＜0.05). The protein levels of RAGE and TLR4 in 25.0 μg/L HMGB1 group were significantly higher than those in other groups (P＜0.05). Marrow mesenchymal stem cells transfected with si-TLR4 antagonized the cell proliferation and secretion of VEGF, bFGF induced by HMGB1. Conclusion HMGB1 promote cell proliferation and secret VEGF, bFGF by binding to its TLR4 receptor.

Abstract:Aim To study the protective effect and possible mechanism of Brazilin on high glucose induced vascular endothelial cell injury, and to provide experimental basis for the treatment of diabetic macrovascular disease with traditional Chinese medicine hematoxylin. Methods Human umbilical vein endothelial cells (HUVEC) were cultured, the concentration of Brazilin was determined by MTT method, high glucose induced injury after joining Brazilin, autophagy body was observed by transmission electron microscopy (TEM), tubule formation test was used to observe angiogenesis, the protein expression of autophagy related genes BECLIN1, LC3-Ⅱ and p62 was detected by Western blot. Results The concentration of Brazilin was 15 mg/L. Transmission electron microscopy showed that the number of autophagic cells in high glucose treatment group was less than that in normal group, but the number of autophagy in the cells of Brazilin group was higher than that in normal group and high glucose treatment group. The expression of BECLIN1 and LC3-Ⅱ protein in high glucose treated group was lower than that in normal group, the expression of BECLIN1 and LC3-Ⅱ protein in Brazilin group was higher than that in high glucose treatment group (P＜0.05); the expression of p62 protein in high glucose treated group was higher than that in normal group, the expression of p62 protein in Brazilin group was lower than that in normal group and high glucose treatment group (P＜0.05). Conclusion Brazilin may play a role of protection in high glucose induced vascular endothelial cell injury through regulating autophagy.

Abstract:Aim To study the effect of anti-aging Klotho protein on oxidative damage induced by hydrogen peroxide (H₂O₂) in human umbilical vein endothelial cell (HUVEC) and its mechanism. Methods The oxidative damage model was built by HUVEC treated by H₂O₂. HUVECs were individed into control group, H₂O₂ damage group, different concentrations (1,0, 100 μg/L) Klotho protein groups and serine-threonine protein kinase (AKT) action group. Cell survival rate was detected by methyl thiazolyl tetrazolium assay. Lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) content were detected by specific Kit. The content of nitric oxide (NO), endothelin-1 (ET-1), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and nuclear factor-kappa B (NF-κB) were detected by enzyme-linked immunosorbent assay. SA-beta galactosidase staining was used to detect cell senescence. Reactive oxygen species (ROS) and cell apoptosis were determined by flow cytometry. Expression of Bcl-2, Bax, NF-κB p65 and p-AKT were detected by Western blot. Results Compared with the control group, the survival rate of HUVEC was significantly decreased, the contents of LDH and MDA were significantly increased, the activities of SOD and GSH were significantly decreased, the ET-1, ICAM-1, VCAM-1, NF-κB, ROS, cell senescence rate and apoptosis rate were significantly increased, the expression of Bax protein and phosphorylation level of NF-κB p65 were significantly increased but Bcl-2 protein and p-AKT/AKT decreased, in H₂O₂ damage group (all P＜0.05). In different concentrations of Klotho protein groups, the cell survival rate was gradually increased, the contents of LDH and MDA were gradually decreased, the activities of SOD and GSH were increased, NO content was increased, the ET-1, ICAM-1, VCAM-1, NF-κB, ROS, cell senescence rate and apoptosis rate were gradually decreased, the Bax protein and phosphorylation level of NF-κB p65 were gradually decreased, the Bcl-2 protein and p-AKT/AKT were gradually increased (all P＜0.05). The results of the above indexes in AKT action group were contrary to those of Klotho protein groups. Conclusions Anti-aging Klotho protein can enhance the HUVEC survival rate after H₂O₂ induced oxidative damage, promote cell function and antioxidation, reduce cell inflammatory reaction, aging and apoptosis. It plays roles through inhibiting Bax, NF-κB p65 and promoting Bcl-2, p-AKT/AKT.

Abstract:Aim To observe the structural changes of human coronary atherosclerotic lesions and the expression of CD40L and matrix metalloproteinase-9 (MMP-9) protein, and to explore the role of CD40/CD40L signaling in the development of human coronary atherosclerosis. Methods 60 cases of human coronary artery with different degrees of atherosclerosis were collected as experimental group, and 12 cases without pathological changes were as control group. HE staining was used to observe the histological structure of coronary artery in the two groups, and image analysis software was used to detect the related indexes of the lesion structure. The expression levels of CD40L and MMP-9 protein were detected by immunohistochemical staining. The relationship between the expression of CD40L and MMP-9 and the structural changes of atherosclerotic lesions were analyzed. Results The expression of CD40L protein was enhanced in all the atherosclerotic coronary artery, and it was mainly expressed in the foam cells of the plaques shoulder and bottom. Moreover, the expression level of MMP-9 protein in the lesion was increased and it was positively correlated with the CD40L expression and the lesion size especially the necrosis size. There was no correlation between the expression level of MMP-9 and the thickness of fibrous cap. The ratio of fibrous cap thickness to the maximum intimal thickness was decreased with the increase of MMP-9 level. Conclusions The expressions of CD40L and MMP-9 protein are significantly enhanced in the human coronary atherosclerotic lesions. CD40L may promote the expression of MMP-9, to strengthen the extracellular matrix decomposition in vascular lesions, so as to promote the development of lesions and the enlargement of necrotic foci, thus the stability of atherosclerotic lesions is decreased.

Abstract:Aim To probe the effect of Intermittent aerobic exercise on Adrenomedullin (ADM) secretion of artery of spontaneous hypertensive rat (SHR), and investigate the mechanism of artery of exercise in the prevention and treatment of hypertension. Methods 30 SHR are separated into two groups:intermittent exercise group (IAE Group) and control group. The IAE group performs 8 weeks intermittent treadmill exercise and their blood pressure are measured before and after exercise by tail pressure of SHR, serum ADM is detected by enzyme linked immunosorbent assay. ADM is expressed in artery by immunohistochemistry. Quantification of specific-receptor activity modifying protein (RAMP2) and calcitonin receptor like receptor(CRLR) in artery ADM are detected by Westernblotting. Results Quantification of specific receptor ADM were significantly lower than control group(P<0.05) and serum ADM in IAE group were significantly higher than control group(P<0.05). The expression of ADM in artery was obviously stronger than control group. The quantity of RAMP2 and CRLR in artery were increased obviously (P<0.05). Conclusion Intermittent aerobic exercise increases the expression of ADM in artery and their specific receptor RAMP2 and CRLR up regulation may be one of the mechanisms of lower SHR blood pressure.

Abstract:Aim To observe the protective effect of Baicalin on vascular endothelial cells induced by oxidized low density lipoprotein (ox-LDL). Methods In vitro cultured human umbilical vein endothelial cells (EAhy926) were divided into control group, ox-LDL group, Baicalin group and different concentrations of Baicalin (5,0 and 100 mg/L)＋ox-LDL groups, cultured 24 h. Cell viability was detected by CCK-8, ELISA was used to detect the level of IL-6 and TNF-α in cell culture supernatant, Western blot was used to detect the expression of apoptosis related protein Bax and Bcl-2. Results Compared to the ox-LDL group, the cell survival rates of 0,0 mg/L Baicalin＋ox-LDL groups were significantly increased (P＜0.05), the protein levels of both TNF-α and IL-6 in cell culture supernatant were decreased significantly (P＜0.05), and the ratio of Bax/Bcl-2 decreased (P＜ 0.05). Conclusion Baicalin protects against endothelial cell injury, which may be achieved by inhibiting inflammatory factors, reducing apoptosis and enhancing cell activity.

Abstract:Aim To investigate the association between low bone mineral density (BMD) and severity of coronary artery lesion patients with non-diabetic coronary heart disease. Methods A total of 156 patients with non-diabetic coronary heart disease (CHD) with chest pain were enrolled in the study, clinical characteristic of patients was recorded, coronary artery lesion was determined by coronary angiography, the patients were grouped according to the number of coronary artery lesions:non-coronary artery lesion group, single coronary artery lesion group, double coronary artery lesion group, three coronary artery lesion group. Coronary artery clacification (CAC) was evaluated by 64 slice spiral CT, patients were grouped according to coronary artery calcification score:no calcification group (＜10 score), mild calcification group (10～100 score), moderate calcification group (101～400 score), severe calcification group (＞400 score). In addition, the bone mineral density (BMD) was measured by dual energy X-ray absorptiometry (DXA), according to the results, patients were divided into osteoporosis group, osteopenia group and normal bone group, and the difference of the degree of coronary artery lesions between the three groups was compared. Results With the severity of coronary artery calcification and coronary stenosis, the incidence of BMD were increased. The severity of coronary artery calcification and coronary stenosis in osteopenia group and osteoporosis group were significantly higher than that in normal group, there were statistically significant differences among the three groups (P＜0.01). Conclusion Low bone mineral density can be considered as an independent factor of coronary artery calcification and coronary stenosis in coronary heart disease patient without diabetes.

Abstract:Aim To observe the relationship between protein kinase C (PKC) activity and anterior tibial artery calcification score in patients with diabetic foot. Methods 60 diabetic patients hospitalized for above-knee amputation in the Department of Orthopedics, Affiliated Hospital of Jiangsu University were recruited from October 2012 to January 2016. The patients were categorized based on the severity of anterior tibial artery calcification, which was assessed by computed tomography (CT), into mild calcification group (0＜calcification score＜100, n＝ 20), moderate stenosis group (100≤calcification score＜200, n＝20) and severe calcification group (calcification score≥200, n＝20). Baseline clinical data regarding sex, age, duration of diabetes mellitus, hypertension status, fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), and lipid profile were collected before the amputation. Von kossa staining, PepTag Assay and Western blot were then performed. Results Similarly with Von Kossa staining, CT scan results showed that calcium deposition in anterior tibial artery plaques of diabetic patients hospitalized for above-knee amputation were enlarged and calcium particles density in moderate and severe groups were stronger than that in mild group. The calcification in all calcification groups were showed as spotty calcification. PepTag Assay, Western blot and Pearson correlation showed that anterior tibial artery calcification score in diabetic patients hospitalized for above-knee amputation was positively associated with PKC activity (r＝0.931, P＜0.001). Further analysis indicated that alpha subtypes of PKC maybe played an important role to promote the evolution of calcification. Conclusion The activation of PKC subtypes may be related with the evolution of calcification in atherosclerotic plaques, so as to further target the mechanism of vascular calcification.

Abstract:Aim To explore the correlation between the initial origin stenotic segment of internal carotid artery and calcification score at siphon segment of internal carotid artery. Methods The CTA images of 216 patients were analyzed retrospectively. Calcification score at siphon segment in internal carotid artery was calculated using agatston’s method, all the cases were divided into calcification 0 score group, calcification 1～199 score group, calcification 200～399 score group, calcification 400～599 score group and calcification ≥600 score group. The initial origin stenotic segment of internal carotid artery was assessed based on North American Symptomatic Carotid Endarterectomy Trial. The relationship of calcification score at siphon segment of internal carotid artery were analyzed with initial origin stenotic segment of internal carotid artery. Results Two hundred and sixteen patients with 432 vascular were examined by CTA. Calcification at the siphon segment in internal carotid arteries had been found in 382. There were 70 vascular in calcification 1～199 score group, 100 vascular in calcification 200～399 score group, 112 vascular in calcification 400～599 score group and 100 vascular in calcification ≥600 score group. There were 18(25.7%), 78(78.0%), 106(94.6), 98(98.0%)vascular stenotic respectively in calcification 1～199 score group, in calcification 200～399 score group, in calcification 400～ 599 score group and in calcification ≥600 score group. Chi-square test statistical analysis showed that calcification score was significantly associated with initial origin stenotic segment of internal carotid artery stenotic (P<0.05). The initial origin stenotic segment of internal carotid artery was mild in calcification 0 score group and calcification 1～199 score group, mild-moderate in calcification 200～399 score group and mainly severe in calcification 400～599 score group and calcification ≥600 score group (P＜0.05) . Spearman rank correlation analysis showed that the extent of internal origin stenotic segment of internal carotid artery were positively correlated with the calcification score at siphon segment of internal carotid artery (r=0.721, P<0.01). Conclusion With the growth of calcification score at the siphon segment in internal carotid arteries the probability of initial origin stenotic segment of internal carotid artery has increased. Detection of calcification score at the siphon segment in internal carotid arteries can be used as the effective basis of head and neck vascular stenosis lesions.

Abstract:Aim To investigate the relationship between serum proprotein convertase subtilisin/kexin type 9 (PCSK9) and small and dense low density lipoprotein cholesterol (sdLDLC) in patients with coronary heart disease (CHD). Methods From March 2014 to December 2014 in the first hospital of Shanxi Medical University, 100 patients with CHD diagnosed by coronary angiography were collected as CHD group, and 67 healthy subjects were served as control group. Lipoprint lipoprotein analyzer was used to measure the LDLC particle size, sdLDLC particle number and the percentage of sdLDLC in LDLC (sdLDLC percentage). Serum PCSK9 level was detected by enzyme-linked immunosorbent assay. Results Compared with the control group, LDLC particle size decreased (264.07±6.78 vs. 267.37±5.15, P＜0.01), sdLDLC particle number increased (5.0±9.5 vs. 4.0±5.0, P＜0.05), sdLDLC percentage increased (5.95%±10.50% vs. 3.70%±5.85%, P＜0.01) in the CHD group. The serum PCSK9 level in CHD group was significantly higher than that in control group (15.48 μg/L vs. 14.95 μg/L, U＝－2.74, P＝0.006). In the CHD group, serum PCSK9 level was positively correlated with sdLDLC percentage and LDLC (r＝0.212, P＝0.034; r＝0.202, P＝0.032). Conclusion Serum PCSK9 level is positively correlated with sdLDLC percentage in patients with CHD, and the inhibition of PCSK9 can prevent CHD.

Abstract:Aim To detect the plasma AnnexinⅤexpression rate in elderly patients with acute coronary syndrome (ACS), and explore the correlation between AnnexinⅤexpression rate and cardiovascuar risk factors, fibrinogen (FIB), D-dimer, platelet aggregation rate (PAR). Methods 156 patients who were successfully examined by coronary angiography were recruited in our hospital from December 2014 to May 2016. These patients were divided into ACS group (n＝88), stable angina pectoris (SAP) group (n＝36) and control group (n＝32). The AnnexinⅤexpression rate and PAR were detected by flow cytometry instrument, the levels of FIB and D-dimer were detected by immunofluorescence method determination. Detailed information were recorded in age, history of smoking, diabetes, hypertension and so on.Different groups were compared to analyse the correlation between the AnnexinⅤexpression rate and cardiovascuar risk factors, FIB, D-dimer, PAR. Results The differences of AnnexinⅤexpression rate in ACS group were statistically significant compared with SAP group and control group (P＜0.05 or P＜0.01), but there was no statistically significant difference between SAP group and control group (P＝0.487). When the area under the ROC curve (AUC) was 0.876, the cut-off point was 29.36%, the sensitivity and specificity of diagnosis of ACS were 80.1% and 79.9%. The AnnexinⅤexpression rate in ACS group had a positive correlation with plasma FIB (r＝0.468, P＝0.047), D-dimer (r＝0.451, P＝0.040), PAR (r＝0.531, P＝0.010), smoking (r＝0.510, P＝0.009), hypertension (r＝0.506, P＝0.012) and diabetes (r＝0.493, P＝0.026). Conclusion The plasma AnnexinⅤexpression rate in elderly patients with ACS were positively correlated with diabetes, hypertension, smoking, FIB, D-dimer and PAR, which may be helpful to predict the occurrence and clinical risk of ACS.

Abstract:Aim To explore the effects of aerobic exercise on 6-minute walk distances (6MWD), the lower limb motor function and serum chemerin in patients with chronic hemiparesis after stroke. Methods 108 patients with chronic hemiparesis after stroke were randomly divided into three groups:drug treatment group, drug treatment combined with aerobic exercise treatment group and aerobic exercise treatment group. Drug treatment group and drug treatment combined with aerobic exercise treatment group were given conventional medical therapy. The patients in drug treatment combined with aerobic exercise treatment group and aerobic exercise treatment group received regulear aerobic exercise using power bicycle each for 30 min, 3 times a week in 3 months. 6MWD, simplified Fugl-Meyer lower limb motor function assessment (FMA), blood pressure, body mass and height were recorded, serum chemerin, C-reactive protein (CRP), homocysteine, biochemistry were determined before and after the 3 months therapies. Results There were no significant difference among the three groups before treatment for 6MWD, FMA scores, serum chemerin, CRP, homocysteine, fasting blood glucose, blood lipids, blood pressure, body mass and body mass index(P>0.05 ). After 3 months treatment, 6MWD, FMA scores in drug treatment combined with aerobic exercise treatment group were significantly increased(P<0.01), serum chemerin, CRP, homocysteine, fasting blood glucose, total cholesterol, low density lipoprotein cholesterol(LDLC), systolic blood pressure and body mass in drug treatment combined with aerobic exercise treatment group were significantly decreased (P<0.05), 6MWD, FMA scores in aerobic exercise treatment group were significantly increased(P<0.01), serum chemerin, CRP, homocysteine, fasting blood glucose, total cholesterol, LDLC, systolic blood pressure and body mass in aerobic exercise treatment group were significantly decreased (P<0.05), 6MWD, FMA scores in drug treatment combined with aerobic exercise treatment group were significantly increased than those in drug treatment group after treatment, and CRP, fasting blood glucose and systolic blood pressure in drug treatment combined with aerobic exercise treatment group were significantly decreased than those in drug treatment group after treatment (P<0.05). Before treatment, chemerin was negatively related with 6MWD(r=-0.279, P<0.01). Multiple stepwise regression analysis revealed that chemerin levels was independently associated with 6MWD (P<0.05). Conclusion Aerobic exercise significantly increase 6MWD, FMA scores, reduce serum chemerin, CRP, homocysteine, fasting blood glucose, blood lipids and blood pressure in patients with chronic hemiparesis after stroke, thereby improve quality of life, inflammatory state and the risk factors related to cardiocerebral vascular diseases in patients with chronic hemiparesis after stroke.

Abstract:Aim To establish systematic methods for studying intravascular lipid metabolism of zebrafish. Methods Oil red O staining, CholEsteryl BODIPY 542/563 C11 fluorescently labelling and blood lipids detecting were used to study intravascular lipid metabolism of embryo, larvae and adult zebrafish and the effect of different diet on blood lipid of zebrafish. Results Intravascular lipid of embryo zebrafish was stained by oil red O staining, and intravascular cholesterol was labeled by CholEsteryl BODIPY 542/563 C11. Increased intravascular lipid of larvae zebrafish incubated in egg yolk was stained by oil red O staining, and increased intravascular cholesterol of larvae zebrafish fed by high cholesterol diet was labeled by CholEsteryl BODIPY 542/563 C11. The serum total cholesterol and triglyceride of adult zebrafish were obviously increased after 7 weeks fat feeding. Conclusion Oil red O staining, CholEsteryl BODIPY 542/563 C11 fluorescently labelling and blood lipids detecting can be applied for zebrafish intravascular lipid metabolism research.

Abstract:Atherosclerosis, the pathological basis of various kinds of cardiovascular diseases, is a kind of disease of multifactorial and multistep disorder involving the whole-body large- and medium-sized arteries. The pathogenesis of atherosclerosis is still not fully understood. There is growing evidence that oxidative stress and autophagy are two key factors in the formation and development of atherosclerosis in recent years at home and abroad. Oxidative stress accelerates the occurrence and development of atherosclerosis through direct oxidative damage and indirect signal mediated injury; Autophagy possesses double functions of resisting and promoting the atherosclerosis. While there is a complicated relationship of cross-linking between them. This paper, specified in the following three aspects separately, that is, the roles of oxidative stress, autophagy, and the complicated relationship of cross-linking between them in atherosclerosis, will provide a new way of thinking in understanding and treatment of the disease.

Abstract:Atherosclerosis is a chronic inflammatory disease. The objective of the clinical use of anti-atherosclerotic drugs is to decrease circulating low density lipoprotein level, increase high density lipoprotein level, and reduce inflammation. However, the morbidity and mortality of cardiovascular disease remain high. Therefore, the identification of unknown therapeutic targets and the development of new anti-atherosclerotic drugs is growing. Exosome is a kind of membrane vesicles derived from late nuclear endosome (also known as polycystic body) secreted by living cells. Exosome contains protein, rRNA, and micro RNA, which are related to the source cells, and it can pass the biological barrier and produce various biological functions. Exosome is expected to become a novel drug delivery pathway and gene therapy vector for the treatment of atherosclerosis.

Abstract:Drug eluting stents (DES) have dramatically decreased the rate of in-stent restenosis, which are widely used in patients with atherosclerosis. However, as research continues, increasing evidences have demonstrated that the risk of DES-related stent thrombosis (ST) has tended to increase, which is closely associated with delayed endothelium coverage. Impaired endothelium could induce platelet adhesion and aggregation, incomplete stent apposition, or neoatherosclerosis development. Thus, we will discuss the detailed mechanisms for the DES-related deendothelialization and ST, and the effects of biodegradable stents on vascular endothelium.

Abstract:Epidemiological studies show that there is a positive correlation between the risk of osteoporosis and the incidence of cardiovascular disease, and hypercholesterolemia plays an important role in the occurrence of osteoporosis. The increase of serum cholesterol and low density lipoprotein cholesterol can lead to the decrease of bone mineral density and the occurrence of osteoporosis. Osteoclast and osteoblast are the main bone metabolism cells to maintain bone homeostasis, and cholesterol plays an important role in bone metabolism. This review summarizes the effects of cholesterol and cholesterol-lowering drugs (statins) on the differentiation, formation and activity of osteoblast and osteoclast, thereby providing a novel strategy for the prevention and treatment of osteoporosis.

Abstract:Glucagon-like peptide-1 (GLP-1) is an incretin hormone whose glucose-dependent insulinotropic actions have been regulated as a novel therapy for glycemic control in diabetes. Emerging evidence indicates that GLP-1 exerts direct effects on specific aspects of cardiovascular disease, such as endothelial dysfunction, inflammation, blood pressure and lipid metabolism. This review will focus on the effects of incretin therapies, including GLP-1 analogs and dipeptidyl peptidase (DPP)-4 inhibitors, on the atherosclerosis disease, and will discuss the potential mechanisms underlying these effects.