Abstract:Aim To investigate the beneficial effects of perindopril on bone marrow-endothelial progenitor cell （EPC） mobilization, neovascularization and cardiac function in diabetic rats after acute myocardial infarction （AMI）, and explore the potential underling mechanism for these effects. Methods High fat diet combined with a low dose of Streptozocin （STZ） was used to induce diabetic models, then left anterior descending coronary artery ligation was performed to induce AMI. Diabetic rats were randomly assigned into perindopril group or control group after surgery （n15 in each group）. The percentage of CD45^－/low+CD133⁺KDR⁺EPC in peripheral blood mononuclear cells was measured by flow cytometry pre-operation and at day1,3,5,7,14,28 post-operation, and the plasma level of vascular endothelial growth factor （VEGF） at the same time points was measured by enzyme linked immunosorbent assay （ELISA） kit. Capillary density in the peripheral area of infarction was determined by CD31 staining. Echocardiagraphy was performed to evaluate cardiac function. The expression and phosphorylation of protein associated with EPC mobilization in bone marrow were determined by Western blot analysis. Results Perindopril treatment could notably improve the impaired ischemia-induced EPC mobilization in diabetic condition, and elevate the tiptop of circulating EPC （103±37/10⁶ vs 58±19/10⁶, P<0.05）. At the same time, the level of plasma VEGF was raised, the expression of Akt and endothelial nitric oxide synthase （eNOS）

Abstract:Aim To study the mechanisms of caveolin-1 （Cav-1） up-regulating the extracellular Ca^2＋-sensing receptor （CaR）-induced endothelial nitric oxide synthetase （eNOS） activation in human umbilical vein endothelial cells （HUVECs）. Methods Cultured HUVECs, the same generation of cells were randomly divided into: （1）control group （2）CaR agonist （spermine, 2.0 mmol/L）＋Ca^2＋ group （3）caveolae structural damage （filipin, 1.5 mg/L）＋spermine＋Ca^2＋ group （4）Cav-1 short hairpin RNA （Cav-1 ShRNA）＋spermine＋Ca^2＋ group （5）vehicle＋spermine＋Ca^2＋ group （6）different concentrations （1.5, 2.0, 2.5 mg/L） filipin groups. Western blotting experiments were performed to detect protein expression of Cav-1, eNOS, phosphorated eNOS （p-eNOS） and expressions of Cav-1 and eNOS membrane proteins. The interaction and co-localization between eNOS and Cav-1 were determined using co-immunoprec-ipitates and immunofluorescence analysis, respectively. Results Different concentrations filipin did not influence the expression of eNOS and p-eNOS protein in HUVECs. In the presence of Ca^2＋, the CaR agonist spermine at concentration of 2.0 mmol/L resulted in an increase in the p-eNOS in HUVECs （P<0.05）, the effect of spermine on the increase of p-eNOS was also completely blocked after acute caveolae disruption with filipin （1.5 mg/L） or transfected with Cav-1 ShRNA （P<0.05）. The expression of the eNOS membrane protein was decreased in HUVECs after cells were treated by filipin （1.5 mg/L） or transfected with Cav-1 ShRNA. Simultaneously, total protein level of eNOS was unaffected. Immunocytochemical results demonstrated that filipin （1.5 mg/L） or transfected with Cav-1 ShRNA decreased eNOS localization in caveolae, increased in the local area surrounding the nucleus. Compared with control group and spermine＋Ca^2＋ group, the interaction of eNOS and Cav-1 in Cav-1 ShRNA group was attenuated （P<0.05）. Conclusions Cav-1 might promote CaR-induced eNOS activation. The mechanisms are involved in the effect of Cav-1 on eNOS localization at the plasma membrane and the inhibition of eNOS translocation to the organelles.

Abstract:Aim To observe effects of resveratrol （Res） preconditioning on miRNA expression signature in rat hearts, and analyse the relationship between Res-mediated cardiac protection and miR-21. Methods The expression profiles of miRNAs in rat hearts after Res preconditioning were detected with a miRNAs microarray chip and the results were confirmed by qRT-PCR. After myocardial ischemia/reperfusion （I/R） injury model was established, myocardial infarct size, percent of myocardial apoptosis and expression of miR-21 were tested. Results miR-21 was one of the most up-regulated miRNAs in hearts by Res preconditioning and its expression was increased more than 2.5 fold compared with the control. The up-regulation of miR-21 was significantly inhibited by antagomiR-21. Cardiac cell apoptosis and myocardial infarct size were significantly decreased by up-regulation of miR-21. Conclusion miRNA signature in rat hearts with Res preconditioning has revealed that multiple miRNAs are regulated by Res. Among them, Res has a protective effect on I/R by reducing cardiac cell apoptosis via miR-21.

Abstract:Aim To investigate the expression of poly ADP-ribose polymerase-1 （PARP-1） and to observe the effect of myocardial infarct size after the application of PARP-1 inhibitor 3-aminobenzamid （3-AB） in the early stage of my ocardial ischemia reperfusion （IR）in rat. Methods Rats （n＝164） were randomly divided into 6 groups: operation groups including operation 15 min, 30 min, 1 h, 2 h, 4 h, 6 h and 24 h group （12 rats in each group）, sham groups including sham 15 min, 30 min, 1 h, 2 h, 4 h, 6 h and 24 h group （6 rats in each group）, operation drug group （n＝14）, operation saline group （n＝12）, sham drug group （n＝6）, sham saline group （n＝6）. The left anterior descending coronary artery （LAD） was ligated for 45 min and reperfused for different time of 15 min, 30 min, 1 h, 2 h, 4 h, 6 h and 24 h, IR model was set up, then the rats were killed, and the expression of PARP-1 in myocardial tissue was detected. Sham group animals received all the surgical procedures described previously, but the LAD was not tied. Drug of PARP inhibitor 3-AB （20 mg/kg, iv） was given to operation drug group and sham drug group and the equal volume of saline was given to operation saline group and sham saline group at 30 min after thoracotomy and 45 min after reperfusion, then the expression of PARP-1 in myocardial tissue and the infarct size were detected. Results The levels of PARP-1 in operation groups were obviously higher than those in sham groups （P<0.05）. The level of PARP-1 in operation drug group was obviously lower than that in operation saline group （P<0.05）. Infarct size in operation drug group and in operation saline group after reperfusion 2 hour was obviously different （P<0.05）. Conclusions The content of PARP-1 gradually increased and dynamically changed in the early stage of myocardial ischemia reperfusion. Content of PARP-1 in myocardial after reperfusion for 2 hours had the most obvious expression. Drug of 3-AB obviously inhibited the level of PARP-1, decreased ischemia reperfusion injury and reduced infarct size. Actively using inhibitors of PARP-1 is significantly important in the early stage of myocardial ischemia reperfusion injury.

Abstract:Aim To investigate the roles of reperfusion injury salvage kinase （RISK） signaling pathway and mitochondrial ATP-sensitive potassium channels （mKATP） in the postconditioning effect of adenosine triphosphate （ATP） for rabbits with myocardial ischemia/reperfusion iniury （IRI）. Methods Sixty white male rabbits were exposed to 40 min of ischemia followed by 180 min of reperfusion. Rabbits were intravenously injected 3 mg/kg of ATP （ATP group） or saline （IRI group） immediately after reperfusion within 30 min. The Wortmannin＋ATP, PD98059＋ATP, and 5-hydroxydecanoic acid sodium salt （5-HD）＋ATP groups were respectively injected with Wortmannin （PI3K inhibitor, 0.6 mg/kg）, PD98059 （ERK1/2 inhibitor, 0.3 mg/kg）, and 5-HD （a mKATP blocker, 5 mg/kg） 5 min before ATP administration. Myocardial infarction size was measured by Evans blue and NBT staining. Myocardial apoptosis index was determined by TUNEL methods. Expressions of myocardial Akt, p-Akt, ERK1/2 and p-ERK1/2 were detected by Western blot. Results The myocardial infarction size and apoptosis index were significantly lower in ATP group than those in IRI group, Wortmannin＋ATP group, PD98059＋ATP group and 5-HD＋ATP group （P<0.01）. Western blot showed that the expressions of p-Akt and p-ERK1/2 were significantly higher in ATP group than those in other four groups （P<0.05）.Conclusions ATP postconditioning attenuated IRI by reducing the myocardial infarction size and apoptosis, which is mediated through activation of RISK signaling pathway and opening of mKATP.

Abstract:Aim To observe the effect of atorvastatin on the autophagy of THP-1 macrophages. Methods The Hank’s solution was used to induce the autophagy of THP-1 macrophages. Cells were randomized into four groups: the blank control group and atorvastatin groups the cells were incubated with normal medium in group Ⅰ, Hank’s solution in group Ⅱ, containing low concentration of atorvastatin （1 μmol/L） in Hank’s solution in group Ⅲ, containing high concentration of atorvastatin （5 μmol/L） in Hank’s solution in group Ⅳ respectively. Indirect immunofluorescence was used to detect LC3-FITC dot clustering. Transmission electron microscope was used to detect the autophagy. Result Compared with the control group, the macrophages autophagic vacuoles of both groups of containing atorvastatin medium occupied a total area of cytoplasm increased significantly （P<0.05）, and the high concentration group was not increased more significantly than the low （P＝0.079）. Conclusion Atorvastatin could promote the autophagy of THP-1 macrophages.

Abstract:Aim To investigate the effects of valsartan on lectin-like oxidized low density lipoprotein receptor 1 （ LOX-1） expression induced by asymmetric dimethylarginine （ADMA） in cultured human umbilical vein endothelial cells （HUVEC）. Methods 15 μmol/L ADMA was added into the cultured HUVEC for 24 h, intracellular reactive oxygen species （ROS） generation was measured by DCFH-DA. NADPH p22phox subunit and LOX-1 mRNA transcription were detected by quantitative competitive reverse transcription-polymerase chain reaction （RT-PCR）. LOX-1 protein expression was detected by cell enzyme linked immunosorbent assay （ELISA）. Results Valsartan significantly decreased intracellular ROS generation, inhibited the transcription of p22phox, LOX-1 mRNA and LOX-1 protein expression compared with ADMA group （P<0.05）, and this effect was in a dose-dependent manner. Conclusions Valsartan inhibited expression of LOX-1 induced by ADMA, involving in inhibiting the expression of p22phox through decreasing intracellular ROS generation. This may be part of the mechanism of its anti-atherosclerotic effect independent of anti-hypertensive effect.

Abstract:Aim To explore the effect of oxidized low density lipoprotein （ox-LDL） on human vascular umbilical vein endothelial cell （HUVEC） autophagy and its mechanism. Methods After treatment with ox-LDL for 24 h, Western blot was used to detect the protein expression of Beclin-1 and microtubule-associated protein 1 light chain 3 （LC3） Reverse transcription polymerase chain reaction （RT-PCR） and Western blot were used to detect Rab4 mRNA and protein expression. After transfection with Rab4 siRNA and Rab4 plasmid, Western blot was used to measure the protein levels of Rab4, Beclin-1 and LC3 induced by 75 mg/L ox-LDL. Results After treatment with ox-LDL for 24 h, the protein expression of Beclin-1 and the ratio of LC3Ⅱ/LC3Ⅰ were increased. The levels of Rab4 mRNA and protein were obviously decreased with a concentration-dependent manner. When transfection with Rab4 siRNA, the protein level of Beclin-1 and the ratio of LC3Ⅱ/LC3Ⅰ induced by ox-LDL were further increased. When transfection with Rab4 plasmid, the increased protein level of Beclin-1 and the ratio of LC3Ⅱ/LC3Ⅰ induced by ox-LDL were attenuated. Conclusion ox-LDL increased HUVEC autophagy via down-regulation of Rab4 expression.

Abstract:Aim To observe the effect of melatonin deficiency on macrophage cholesterol efflux and the risk of atherosclerosis in pinealectomized rats. Methods Melatonin deficiency rats （n＝16） were created by pinealectomy （Px）, and compared with sham-operated rats （n＝14）. Blood was drawn at the 0^th week and the 12^th week after surgery to measure serum lipids, glucose and insulin levels. Macrophages were collected at the 0^th and 12^th weeks to measure cholesterol efflux rate and ATP-binding cassette transporter A1 （ABCA1） expression. Results At the 12^th week after surgery, the body weight, serum triglyceride （TG）, very low density lipoprotein cholesterol （VLDLC）, free fatty acide （FFA） and glucose levels were prominently changed in Px rats compared to those in sham-operated rats at the 12^th week （P<0.05）. The ABCA1 mRNA expression was significantly decreased in Px group compared to sham-operated group （P<0.01）. The differences of serum-induced and apolipoprotein A1-induced cholesterol efflux rates between 0^th and 12^th weeks in Px group were both significantly lowered compared to those in sham-operated group （P<0.01）. Conclusions Melatonin deficiency promotes the metabolism abnormality of blood lipids and glucose, and attenuates ABCA1-mediated cholesterol efflux.

Abstract:Aim To discusse the relationship between the number and function of early and late endothelial progenitor cell （EPC） in peripheral blood and the carotid stenosis （CS）. Methods 60 cases were included into the group of objects, and divided into group of 40 patients with carotid artery stenosis （mild stenosis in 20 cases, severe stenosis in 20 cases）, normal control group of 20 cases. The blood was extracted from the patients’ femoral artery in the procedure of cerebrovascular digital subtraction angiography, mononuclear cells were isolated from peripheral blood by density-gradient centrifugation and were cultured for 7 days and 21 days to be identified as early endothelial progenitor cells and late endothelial progenitor cells, colony counting the number of early EPC and late EPC. Proliferation and migration were determined by MTT assay and modified Boyden. The two types of EPCs adhesion assay were performed by replating those on fibronectin-coated dishes, then adherent cells were counted. Results Smoking, high blood pressure and triglycerides, low density lipoprotein in carotid stenosis groups were significantly higher than those in the control group, high-density lipoprotein cholesterol （HDLC） was lower than those of the control group （P<0.05） the difference of age, sex, blood sugar, total cholesterol compared with controls, was not statistically significant （P>0.05）. Compared with controls, the number and function of early EPC, late EPC in carotid stenosis group was decreased, the number and function changes of late EPC were negatively correlated with the degree of cerebral stenosis（P<0.05）. Conclusions Decreased late EPC colonies amount and functional impairment can be observed in patients with carotid artery stenosis. The number and function changes of late EPC were negatively correlated with the degree of cerebral vascular stenosis. Detection of late EPC number and function can be indirect prediction of carotid stenosis severity.

Abstract:Aim To assess the correlation between the peripheral blood T cell subgroup proportion and the degree of coronary atherosclerosis in patients with coronary heart disease to provide the evidence for the T lymphocyte mediating immune inflammation, and inducing plaque progression. Methods Fifty-seven patients were enrolled after routine and coronary angiography examinations between June 2012 and December 2012. The proportion of peripheral blood CD3⁺ cell in peripheral blood lymphocyte, and CD4⁺, CD8⁺ cell in the T lymphocyte, and CD4⁺CD25⁺Treg, CD4⁺CD28^－T cell in the CD4⁺T cells, were detected by flow cytometry using five-color fluorescent markers. Correlation between the peripheral blood T lymphocyte subgroup and the degree of coronary atherosclerosis （modified Gensini standard） was analyzed. Results The proportion of peripheral blood CD3⁺ cell in stable angina pectoris（SAP） group, unstable angina pectoris（UAP） group and acute myocardial infarction （AMI） group were significantly higher than those in control group （all P<0.05）. The proportion of CD4⁺ cell and CD8⁺ cell in UAP group and AMI group were significantly different compared with those in control group and SAP group （all P<0.05）. The proportion of CD4⁺CD25⁺ Treg and CD4⁺CD28^－ cell in UAP group and AMI group were significantly different compared with those in control group and SAP group （all P<0.05）. The peripheral blood CD3⁺ cell were positively correlated with Gensini score（r0.608,P<0.01）. The CD4⁺ cell were positively correlated with Gensini score （r0.624,P<0.01）. The CD8⁺ cell were negatively correlated with Gensini score （r－0.548,P<0.01）. The CD4⁺CD25⁺Treg were negatively correlated with Gensini score（r－0.617,P<0.01）. The CD4⁺CD28^－T cell were positively correlated with Gensini score（r0.399,P<0.01）. Conclusions T lymphocyte subgroup plays an important role in the developmant and progression of atherosclerosis, and has certain prospective value in the clinical evaluation of the severity of the coronary disease.

Abstract:Aim To observe clinical effect and explore preliminary mechanism of Oleanolic acid strengthening atorvastatin lipid-lowering in patients with hyperlipidemia. Methods 107 cases of patients with hyperlipidemia were divided into atorvastatin therapy group or combination therapy group of atorvastatin and oleanolic acid, and the course of therapy was 3 months. The concentration of serum TC, LDLC , TG, HDLC were detected before and after treatment. The changes in serum lipid levels before and after treatment were compared between the two groups. Serum PCSK9 concentrations were detected by ELISA before and after treatment. Results General data including TC, LDLC, TG, HDLC were matched between atorvastatin therapy group and combination therapy group of atorvastatin and oleanolic acid. There were no significant difference in all compared data between two groups. All of two therapy protocols achieved remarkable results. Compared with the same group before treatment, TC and LDLC and TG were significantly decreased after treatment in two groups, and the difference was statistically significant （P<0.05） Compared with atorvastatin therapy group, TC and LDLC decreased more obviously in combination therapy group of atorvastatin and oleanolic acid, the difference was statistically significant （P<0.05）. The initial serum PCSK9 concentration difference was not statistically significant （72.4 ± 4.2 μg/L vs 71.1 ± 3.9 μg/L, P>0.05） in two groups. After treatment, in atorvastatin therapy group, serum PCSK9 concentration increased by about 30%, the difference was significant （72.4 ± 4.2 μg/L vs 95.1 ± 3.7 μg/L, P<0.01） compared with before treatment in combination therapy group, atorvastatin and oleanolic acid serum PCSK9 concentrations was slightly higher （71.1 μg/L± 3.9 vs 77.6 ± 4.4 μg/L） compared with before treatment, the difference was non-significant But in atorvastatin therapy group serum PCSK9 concentrations were significantly higher than combination therapy group with atorvastatin and oleanolic acid, the difference was significant （95.1 ± 3.7 μg/L vs 77.6 ± 4.4 μg/L, P<0.05）. Spearman correlation analysis was performed among the patients’ plasma total cholesterol, HDL cholesterol,TG, and LDL cholesterol and their circulating PCSK9 concentrations. PCSK9 correlated positively and significantly with both total cholesterol （r0.76, P0.001） and LDL cholesterol （r 0.72, P0.001）, but not with HDL cholesterol or TG （data not shown）. Conclusion Oleanolic acid can enhance atorvastatin lipid-lowering effect in hyperlipidemic patients, which may relate to oleanolic acid inhibiting PCSK9 expression.

Abstract:Aim To observe the changes of postprandial lipid levels and serum asymmetric dimethyl arginine levels, brachial artery endothelial function after taking fenofibrate in diabetic patients with non-alcoholic fatty liver （NAFL） and normal fasting lipid levels. Methods 110 normal fasting lipid patients with type 2 diabetes were randomly selected and divided into type 2 diabetes with NAFL and type 2 diabetes without NAFL, including 56 patients and 54 patients respectively. Both groups were measured and compared in fasting lipids, blood glucose, glycosylated hemoglobin, serum asymmetric dimethyl arginine levels, alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, 4 hours after the meal and vascular endothelial function. Ultrasound was used to test brachial artery endothelial function, patients in type 2 diabetes with NAFL group were randomly divided into treatment group and control group, and the control group received conventional therapy, while the treatment group were given fenofibrateon 0.2 g daily orally treatment for 6 months on the basis of conventional therapy. After treatment review, these indicators were compared with those before treatment. Results Postprandial lipids, serum asymmetric dimethyl arginine, aspartate aminotransferase, alanine aminotransferase levels in type 2 diabetes with NAFL group were significantly higher than those in type 2 diabetes without NAFL group, and the difference was statistically significant （P<0.05）. 4 hours after treatment postprandial lipids, serum asymmetric dimethyl arginine levels in treatment group decreased, brachial artery endothelium-dependent function increased, the difference was statistically significant in the control group before and after treatment. Conclusions Fenofibrate can improve the vascular endothelial function in diabetic, NAFL patients with postprandial triglyceride hyperlipidemia.

Abstract:Aim All the patients had received digital subtraction angiography to investiagte the relationship between the clinical features of carotid transient ischemic attacks and intracranial or extracranial angiostenosis. Methods The frenquency of senosis of the intra-cranial and extracranial arteries in digstal subtraction angiography of 251 patients with carotid transient ischemic attacks was caiculated. The frequency of stenosis of arteries in various age groups was compared. Results Among the 251 patients, cerebral artery stenosis was found in 248 （98.8%）. Totally 688 arteries were detected. Anterior circulation lesions in 587 （85.3%）, posterior circulation lesions 101 （14.7%）. In yonug group, the frequency of stenosis of intracranial artery was higher than extracranial artery, while in the old group, the frequency of stenosis of extracranial artery was higher than intracranial artery. In the old group, the frequency of stenosis of extracranial artery was higher than the middle-age group and young group, while in the middle-age group, the frequency of stenosis of extracranial artery was higher than young group. Conclusion In the study, cerebral artery stenosis distributes characteristicly with age.

Abstract:Aim Obtain purified moesin protein by recombinant,purified recombinant moesin protein was plated as coating antigen of indirect ELISA. And discussion on the relationship between momesin antibody and atherosclerosis-related diseases. Methods A pair of primers were designed according to the sequence of the moesin. The moesin gene was amplified by PCR. PCR products were then inserted into a prokaryotic expression plasmid, Using isopropyl thiogalactoside （IPTG） induced expression in the appropriate temperature and conditions. Recombinant moesin protein was analyzed by SDS-PAGE. Recombinant moesin protein will be purified. Purified recombinant moesin protein was applied to establish the indirect ELISA. Adsorption assay in 120 patients（20 patients with acute coronary syndrome,30 patients with primary hypertension,20 patients with carotid atherosclerosis,20 patients with diabetes and 30 patients with hyperlipidemia） with diseases related to atherosclerosis anti-moesin antibody by ELISA, compared the positive rate of anti-moesin antibody of blood. Results The expression product was recombinant moesin by SDS-PAGE2） The optimal antigen concentration was 4 mg/L, the optimal antibody dilution was 1∶100, the optimal HRP-IgG dilution was 1∶20 000. In 120 cases of diseases related to atherosclerosis, positive rate is higher protein antibody against membrane process, up to 25%～70%, significantly higher than that of normal control group 5% （P<0.01） acute coronary syndrome group, the positive rate of 70%, higher than the other groups （P<0.05）, the difference between other subtypes of disease no significant （P>0.05）. Conclusion Successfully expressed the recombinant human moesin protein Establish the best indirect ELISA of Purified recombinant moesin protein was plated as coating antigen detect moesin antibody Moesin antibodies in patients with atherosclerotic disease associated with high detection rate.

Abstract:Aim To observe the characteristics of coronary artery calcium （CAC） and coronary artery calcium score（CACS） in the village population in Yunnan province. Methods Coronary calcium scan with 16-MDCT was performed in 174 cases sampled randomly from the village population in Yunnan province. Coronary artery calcium score was calculated. The characteristics and difference of CAC and CACS were compared between groups of gender, age and race. Results The positive rate of CAC in 174 samples was 22.4% and 39 samples with CACS≥1, the positive rate of CAC in 51～60 years group and 61～71 years group was 15.5% and 34.4% respectively and the CACS was 11.2±52.4 and 38.0±82.0. The difference of CAC and CACS in these groups had remarkable statistical significance （P<0.05）, however, these index between the gender and race had no statistical significance, the positive rate of CAC in coronary artery was LAD＞LCX＝RCA＞LM. Conclusions CAC and CACS had age differences in age group of 51～71 years of the village population in Yunnan. The highest incidence of CAC was in the 1eft anterior descending artery, followed by 1eft circumflex artery and right coronary artery.

Abstract:Endothelial microparticles are the vesicles without nucleus shed from the plasma membranes of endothelial cells that are activated or undergoing apoptosis, which is involved in many signal transduction in vivo. The action of endothelial microparticles detaching from the endothelial cell is regulated precisely by a variety factors in vivo，and which play a key role in the occurrence and development of cardiovascular diseases. In this paper the structure, function of the endothelial microparticles and their association with cardiovascular diseases, especially the clinical significance of endothelial microparticles in cardiovascular diseases risk assessment, monitoring and treatment, combined with the current research progress are reviewed.

Abstract:Ischemia reperfusion injury is inevitable in the treatment for acute myocardial infarction. It is a complicated inflammatory response involved by variety of inflammatory cytokines and cellular pathways,which involved in oxidative stress,mitochondrial damage and calcium overload. To make the injury minimize,many researhes were carried on to explore the specific mechanisms. The discovery of new cytokines and target sites provide us new orientation for clinical treatment.

Abstract:The voltage-dependent anion channel （VDAC）, a mitochondrial membrane channel protein located in the outer of mitochondrial membrane, is the main pathway between mitochondria and cytoplasm exchanging ADP, ATP, and other metabolites, and plays an important role in mitochondrial metabolism and cell growth. A growing evidence showed that VDAC was increased in cardiovascular diseases including myocardial ischemia and reperfusion, diabetes, heart failure, hypertension and atherosclerosis. The abnormal state of VDAC will result in cell death by inducing calcium cycling dysfunction and oxidative stress. And VDAC has become a hot topic in the field of cardiovascular diseases research. In this article, we will introduce the molecular function and regulation of VDAC and its role in cardiovascular diseases.

Abstract:Since 1931 deuterium has been founded, the biological effect of deuterium depleted water has aroused wide concern on all kinds of living organisms. Because biological process of living organisms is very sensitive on concentration changes of the deuterium, reduced deuterium concentration can stimulate growth of living organism. And the high deuterium concentration can cause different kinds of damage. In this paper, advances of deuterium depleted water in medicine are summarized, including cardiovascular disease, diabetes mellitus, oxidative stress, aging, radiation, and tumor.