Abstract:Aim To investigate the roles of the interaction between reactive oxygen species （ROS） and ATP-sensitive K^＋ （K_ATP） channel in high glucose （HG）-induced cardiac muscle cells injury.Methods The expression levels of K_ATP channel protein and cleaved caspase-3 protein were determined by Western blot assay. The intracellular level of ROS was detected by 2',7'-dichlorfluorescein-diacetate （DCFH-DA） staining and fluorescence microscopy. The cell viability was measured by cell counter kit-8 （CCK-8） assay. The number of apoptotic cells was tested by Hoechst 33258 nuclear staining and photofluorography. Mitochondrial membrane potential （MMP） was examined by JC-1 staining.Results After H9c2 cells were treated with 35 mmol/L glucose （high glucose, HG） for 24 h, the expression level of K_ATP channel protein was significantly reduced. Pretreatment of the cells with 1000 μmol/L N-acetyl-L cysteine （NAC, a scavenger of ROS） for 60 min before HG exposure obviously reduced the HG-induced inhibitory effect on the expression of K_ATP channel protein. Meanwhile, pretreatment of the cells with 100 μmol/L diazoxide （DZ, a mitochondrial K_ATP channel opener） or 50 μmol/L pinacidil （Pin, a none-selective K_ATP channel opener） markedly inhibited HG-induced accumulation of intracellular ROS in cardiac cells. On the other hand, 1000 μmol/L NAC, 100 μmol/L DZ and 50 μmol/L Pin obviously inhibited HG-induced cardiac muscle cells injury, leading to an increase in cell viability, a decrease in number of apoptotic cells, cleaved caspase-3 expression and MMP loss respectively.Conclusion In HG state, there is an interaction between ROS and K_ATP channel, which plays an important role in the HG-induced injury in cardiac muscle cells.

Abstract:Aim To detect the expression of CC chemokine receptor 2 （CCR2） in collateral vessels induced by high fluid shear stress in rabbit hindlimb and its relationship with monocyte and macrophage.Methods Ten rabbits were operated on left femoral artery ligation, on the right side, the femoral artery was ligated unilaterally and its distal end was anastomosed with femoral vein. After 7 days, the animals were sacrificed. The expression of CCR2, MCP-1 and CD11b was detected by corfocal immunofluorescence. Forelimb vessel was used as normal controls.Results In normal arteries, the expressions of CCR2 and MCP-1 were very weak and only presented in tunica media and adventitia, CD11b was low in the adventitia. In only ligated-side collateral vessels, the expressions of CCR2 and MCP-1 were increased in all layers of vessel wall, and the expression of CD11b in adventitia was increased. In ligation plus anastomosed, the expressions of CCR2, MCP-1 and CD11b were significantly up-regulated （P<0.05）.Conclusions The expression of CCR2 was up-regulated in collateral vessel growth induced by high fluid shear stress in rabbit hind limb, promoting the collateral vessel growth through MCP-1/CCR2 pathway that enables monocytes accumulation to mature form of macrophage.

Abstract:Aim To investigate the role of endoplasmic reticulum stress （ERS）-mediated apoptosis in atherosclerotic calcification of diabetic apolipoprotein E gene knocked-out （ApoE^－/－） mice.Methods 6 weeks old male ApoE^-/- mice were first rendered diabetic by intraperitoneal injection of streptozotocin （STZ） for 5 days ［40 mg/（kg·d）］. After 2 weeks, the blood glucose level ＞3000 mg/L mice were included in this study, and then were given a semi-synthetic high-fat diet （HFD）, plus daily tail vein injection of carboxy methyl lysine （CML） ［10 mg/（kg·d）］. The mice were euthanized at 0 month （group 0M, n＝10）, 2 months （group 2M, n＝10）, and 4 months （group 4M, n＝10） after the triple administration of STZ-CML-HFD. Related detection and analysis were carried out for each group of mice. Results Morphological analysis showed that early atherosclerotic plaques appeared at 2 months after the triple administrations of STZ-CML-HFD, and that typically advanced plaques with extensive calcification lesions, abundant cholesterol crystals, and proliferative collagen were formed at 4 months after the triple administrations of STZ-CML-HFD. The intrinsic phenotype （SM22α） of aortic smooth muscle cells was gradually lost, and osteoblast-like phenotypes （bone morphogenetic protein-2, core binding factor α1, alkaline phosphatase） were increased. CML deposition signal and the expression of receptor for advanced glycosylation end product （RAGE） in the aortic wall were mainly restricted in the atherosclerotic plaques. Western blot assay showed the expressions of CML, RAGE and CD36 in aortic wall of diabetic ApoE^－/－ mice were significantly up-regulated, but the expression of ATP binding cassette transporter A1 firstly displayed a compensated increase and then reduced near the baseline. Experiment of TUNEL staining and cleaved caspase-3 immunohistochemical staining found intra-plaque cells apoptotic rate rised with the progression of diabetic atherosclerosis. Immunohistochemical location analysis showed glucose regulated protein 78 （GRP78）, a molecular chaperone of ERS and C/EPB homologous protein （CHOP） were mainly restricted in the lipid poor of atherosclerosis. Furthermore, compared with CHOP, the distribution signal of GRP78 in group 4M appeared more basal in lipid pool. Western blot semi-quantitative analysis found that the related indexes of ERS （GRP78, phosphorylated protein kinase RNA-like endoplasmic reticulum kinase, phosphorylated eIF2α, activating transcription factor 4, CHOP） were up-regulated with the extension of diabetic course in ApoE^－/－ mice.Conclusions STZ-CML-HFD combined intervention for 4 months can induce atherosclerotic calcification of diabetes in ApoE^－/－ mice. CML/RAGE may firstly start-up ERS-mediated apoptosis, and then cause to happen the calcification cascade signal.

Abstract:Aim To investigate whether miR-31-5p could promote progression of atherosclerosis via inhibiting insulin-degrading enzyme （IDE）.Methods To establish the effect of miR-31-5p on the 3’UTR of human IDE, the bioinformatics analysis and dual luciferase assay were performed. To investigate the impact of miR-31-5p on IDE expression and cholesterol homeostasis, cultured THP-1 macrophages and THP-1 macrophage-derived foam cells were transfected with miR-31-5p mimic or inhibitor. ApoE^－/－ mice administered high-fat diet （HFD） were treated by miR-31-5p agomir. The IDE protein levels were measured by Western blot analysis. The plasma lipid levels in ApoE^－/－ mice were measured by ELISA kit. The hepatic lipid deposition and atherosclerotic lesions in ApoE^－/－ mice were measured by oil red O.Results IDE was a potential target of miR-31-5p according to the results of bioinformatics analysis and dual luciferase assay. IDE protein levels were remarkably down-regulated by miR-31-5p in THP-1, hepatic and aortic tissue（P<0.05）. The lipid levels in THP-1 macrophage-derived foam cells and ApoE^－/－ mice plasma were significantly up-regulated by miR-31-5p（P<0.05）. Meanwhile, a significant increase of hepatic lipid deposition and atheromatous plaque formation in ApoE^－/－ mice were induced by miR-31-5p（P<0.05）.Conclusion miR-31-5p promotes progression of atherosclerosis via inhibiting insulin-degrading enzyme.

Abstract:Aim To investigate the effects of OPN-002-siRNA transfection on intimal hyperplasia and osteopontin （OPN）, transforming growth factor-β1 （TGF-β1）, proliferating cell nuclear antigen （PCNA） expression after carotid balloon injury in rat.Methods Through preliminary experiment, OPN mRNA in cultured vascular smooth muscle cells was tested by real-time reverse transcription polymerase chain reaction （real-time RT-PCR）, and OPN-002-siRNA was determined as the most sensitive sequence and used as transfected siRNA in the subsequent animal experiments. Seventy-two rats were randomly divided into four groups: sham group, balloon injury group, OPN-scramble-siRNA （OPN-SCR-siRNA） group and OPN-002-siRNA group. Changes of intimal hyperplasia and OPN, TGF-β1, PCNA expressions were detected by immunofluorescence, hematoxylin-eosin （HE） staining, real-time RT-PCR and Western blot, and also the effect of OPN-002-siRNA was studied on them.Results （1）There was no apparent neointima on the 3rd day after balloon injury. Intima began to thicken on the 7th day after injury, and intimal thickening was significant on the 14th day. （2）The expression of OPN, TGF-β1 mRNA and protein started to increase on the 3rd day and persisted until the 14th day. The expression of PCNA mRNA and protein started to increase on the 3rd day, peaked on the 7th day, decreased on the 14th day. （3）Compared with balloon injury group and OPN-SCR-siRNA group, the neointima thickness decreased significantly on each time point in OPN-002-siRNA group （P<0.001）, and both mRNA and protein expression of OPN, TGF-β1 and PCNA reduced significantly on each time point in OPN-002-siRNA group （P<0.001）.Conclusion OPN-002-siRNA can inhibit intima hyperplasia after artery injury by decreasing the expression of OPN, TGF-β1 and PCNA.

Abstract:Aim To study the effect of fluoxetine on serotonin-induced RhoA signalling pathway in pulmonary arterial smooth muscle cells.Methods The pulmonary arterial smooth muscle cells of rat were exposed to serotonin for 48 h with or without fluoxetine or fasudil. Then pulmonary arterial smooth muscle cells proliferation was tested by 3-［4,5-dimethylthylthiazol-2-yl］-2,5 diphenyltetrazolium broide assay. The cellular extracts were prepared for coimmunoprecipitation or Western blot of RhoA signalling pathway.Results Serotonin promoted pulmonary arterial smooth muscle cells proliferation, increased RhoA serotonylation, RhoA membrane translocation, Rho kinase 2 protein expression and myosin phosphatase target subunit 1, extracellular regulated protein kinase and protein kinase B phosphorylation. Fluoxetine inhibited these changes dose-dependently. However, fasudil did not inhibit increased RhoA serotonylation induced by serotonin.Conclusion Fluxetine inhibited serotonin-induced pulmonary arterial smooth muscle cells proliferation via inhibition of RhoA signalling pathway.

Abstract:Aim To investigate the effect of ten-eleven translocation oncogene family member 2 （TET2） on oxidized low density lipoprotein （ox-LDL）-treated human umbilical vein endothelial cell （HUVEC） proliferation and migration.Methods HUVEC was incubated with 0, 25, 50, 75 ox-LDL mg/L respectively for 24 h, and Western blot was used to detect HUVEC TET2 protein expression. Methyl thiazolyl tetrazolium （MTT） method was used to detect the effect of TET2 on ox-LDL-treated HUVEC proliferation. Transwell experiment and scratch experiment were used to detect the effect of TET2 intervention on ox-LDL-treated HUVEC migration. Immunofluorescence was used to detect the effect of TET2 intervention on HUVEC cytoskeleton, and Western blot was used to detect the expressions of total Rac1 （tRac1） and phosphorylated Rac1 （pRac1） in HUVEC.Results Oxidized low density lipoprotein inhibited HUVEC TET2 expression with a dose-dependent manner. TET2 overexpression improved the ox-LDL-induced HUVEC proliferation and migration inhibition, while TET2 low expression （TET2 shRNA） further inhibited HUVEC proliferation and migration. Immunofluorescence showed that ox-LDL induced the formation of HUVEC peripheral compact zone. TET2 overexpression inhibited the formation of compact zone induced by ox-LDL, while TET2 shRNA strengthened the compact zone formation. Western blot showed that ox-LDL inhibited the expression of Rac1 protein in HUVEC. TET2 overexpression increased the levels of tRac1 and pRac1 in HUVEC, while TET2 shRNA further decreased the levels of tRac1 and pRac1.Conclusion Oxidized low density lipoprotein can inhibit the expression of TET2, which regulate HUVEC cytoskeleton, so as to inhibit the proliferation and migration of HUVEC.

Abstract:Aim To observe the effect of myocardial ischemia on the expression of heart type fatty acid binding protein （H-FABP） in myocardium of rats and to explore its possible molecular mechanism.Methods SD rats were randomly divided into sham operation group and myocardial ischemia 1, 3, and 7 days groups. A model of myocardial ischemia was constructed by ligating the left anterior descending coronary artery. The heart function was assessed by detecting the cardiac hemodynamic parameters left ventricular systolic pressure （LVSP）, left ventricular end-diastolic pressure （LVEDP） and ＋dp/dt_max, －dp/dt_max using PowerLab instrument. The mRNA and protein expressions of H-FABP and peroxisome proliferator-activated receptor ɑ （PPARɑ） in myocardium were detected by quantitative PCR and Western blot respectively. The survival rate of rats was observed.Results Compared with the sham operation group, hemodynamic parameters LVSP, ＋dp/dt_max, －dp/dt_max were decreased and LVEDP was increased continuously at 1, 3 and 7 days after myocardial ischemia （P<0.01）. Results from quantitative PCR and Western blot showed that the expression of H-FABP was up-regulated at the 1 day after ischemia, but started to fall at 3 days and returned to the baseline level at 7 days after ischemia. The expression of PPARα was continuously decreased at 1, 3 and 7 days after ischemia, however, its phosphorylation was increased at 1 day and then fell subsequently. The survival rate of myocardial ischemia group was decreased significantly compared with the sham operation group.Conclusions The expression of H-FABP in ischemic myocardium is elevated at the earlier stage, which is related to the increased phosphorylation of PPARα. Then, the expression of H-FABP is decreased, which may be related to the down-regulation of the expression and phosphorylation of PPARɑ.

Abstract:Aim To explore risk factors in the progression of carotid atherosclerosis, provide the basis for stroke prevention.Methods By random cluster sampling method, take the permanent residents aged 60 to 70 years in Renqiu as the targets. By taking face to face health questionnaire, anthropometric measurements, laboratory testing, vascular ultrasound examination of the neck, 5 010 cases are screened. Select 2 456 cases whose carotid ultrasound examinations showed plaques and stenosis for the study, observe their dynamic progression of stenosis and stenosis aggravating , and analyze risk factors of carotid atherosclerosis in progress.Results Within the 2 456 cases who prompted plaques and stenosis in carotid ultrasound in 2012, there were 223 cases which have suggestive carotid stenosis and stenosis aggravating in 2013 , among them, 123 cases were male （5.0%）, 100 cases were female （4.1%） Their associated risk factors as history of hypertension, diabetes mellitus, hyperlipidemia, cerebrovascular disease, smoking, passive smoking, excessive drinking, obesity, lack of physical exercise, atrial fibrillation, coronary heart disease, peripheral vascular, periodontal disease constituent ratio were 50.0%, 20.3%, 23.9%, 20.1%, 40.1%, 24.0%, 10.6%, 19.5%, 15.6%, 2.0%, 16.1%, 6.0%, 8.3%. Multivariate logistic regression analysis showed that smoking, systolic blood pressure, LDLC, cerebrovascular disease are independent risk factors in carotid atherosclerosis progression （P<0.05）.Conclusion One of the main causes of ischemic cerebrovascular disease is atherosclerotic carotid stenosis, and actively promoting smoking cessation campaign, effective control of blood pressure, LDL-C, especially those with a history of stroke population, can effectively control and reduce cerebrovascular disease occurring.

Abstract:Aim To evaluate the association of the central retinal arteriolar equivalent （CRAE） that reflects microcirculation, with brachial-ankle pulse wave velocity （baPWV） that reflects aortic stiffness.Methods In this cross-sectional study, we identified the cardiovascular risk factors in 2169 subjects with an age of 30+ years using a health questionnaire, physical examinations and laboratory examinations. We evaluated the aortic stiffness using non-invasive baPWV and assessed the microcirculatory alterations with CRAE, which were measured using fundus photography and semi-automatic quantitative software, respectively.Results The baPWV gradually increased with the increase in mean age, systolic blood pressure, diastolic blood pressure, arterial blood pressure, pulse pressure, BMI, LDLC. The baPWVs in the diabetic and hypertensive subjects were higher than those in the non-diabetic or non-hypertensive subjects. The increase in baPWV was correlated with an increased likelihood of the central retinal artery narrowing.Conclusions Elevated baPWV correlates with reduced CRAE. Such a finding supports macrocirculation- and microcirculation-associated hypotheses.

Abstract:Aim To investigate the correlation between health-related quality life （HRQL） and risk factors in non-diabetic premature coronary heart disease （CHD） man.Methods 215 non-diabetic man patients （age fewer than 50） were selected from cardiology department （Sun Yat-sen Memorial Hospital of Sun Yat-sen University） from January 2012 to January 2015. All subjects were diagnosed by coronary angiography and divided into two groups according to the percentage of coronary artery stenosis as follows: 104 cases with coronary artery stenosis above 50% （age 43.04±4.69, CHD group） and 111 cases with coronary artery stenosis less than 50% （age 42.92±4.30, Healthy control group）. Clinical data and health-related quality information were collected and analyzed by SPSS 18.0.Results 1） Hypertension, hyperlipidemia, smoking, family history, diastolic blood pressure and systolic blood pressure were significantly higher in the CHD group than that of the healthy control group （P<0.05） 2） The proportion of low education, stress pressure and excess fatigue were significantly higher in the CHD group than that of the healthy control group （P<0.05） 3） Smoking, hypertension, high pressure and excess fatigue significantly increased the incidence of coronary heart disease in non-diabetic man patients after adjusting the relative risk factors, which included smoking, drinking, hypertension, hyperlipidemia, hyperuricemia, the family history of coronary heart disease, low education, stress pressure and excess fatigue. The odds ratio （OR） and 95% CI for smoking, hypertension, stress pressure and excess fatigue were 5.005 （2.096, 11.954）, 3.704 （1.466, 9.355）, 2.635 （1.309, 5.302）, 2.594 （1.192, 5.648） respectively （P<0.05）.Conclusion Our data suggest that smoking, hypertension, stress pressure and excess fatigue are the risk factors of premature CHD in non-diabetic man, and smoking is the most significant risk factor in this study.

Abstract:Aim To research the therapeutic effect of load-dose clopidogrel combined with aspirin on transient ischemic attack （TIA） of posterior circulation.Methods A total of 84 patients with transient ischemic attack of posterior circulation hospitalized at our hospital between May 2011 and October 2013 were randomly bisected into therapy group and control group. 42 patients in control group were administrated with aspirin, while 42 patients in therapy group were administrated with load-dose clopidogrel combined with aspirin. After 4 weeks’ treatment, curative effects, platelet count and cerebral microbleeds （CMB） were compared between the two groups.Results After 4 weeks’ treatment, therapy group showed better curative effects than those in control group（incidences of significant efficiency: 57.14% vs. 35.71%, P<0.05 incidences of efficiency: 85.71% vs. 54.76%, P<0.05）. The platelet count and CMB of the two groups before and after the treatment had no statistical difference （P>0.05）. Neither group had systemic bleeding and other serious adverse events.Conclusions Load-dose clopidogrel combined with aspirin has a significant curative effect on transient ischemic attack of posterior circulation. Efficiency and safety suggest the worth of clinic promotion.

Abstract:Aim To study the diagnostic value of brachial-ankle pulse wave velocity （baPWV） and ankle-brachial index （ABI） for early atherosclerosis （As） in patients with hypertension.Methods 2400 cases of patients with hypertension were collected from January 2010 to December 2014 in our hospital. These patients were divided into two groups: non-As hypertension group （1200 cases） and As hypertension group （1200 cases）. 1248 cases of healthy examination persons in the same period were regarded as the control group. baPWV, ABI and intima-media thickness （IMT） were detected and compared in the three groups.Results Compared with the control group, the levels of baPWV, SBP, DBP, TG and LDLC were significantly increased in the non-As hypertension group and the As hypertension group （P<0.05） Compared with the non-As hypertension group, the levels of baPWV, TG and LDLC were significantly increased in the As hypertension group （P<0.05）. Compared with the control group, the levels of ABI and HDLC were obviously decreased and the IMT thickening rate was significantly increased in the As hypertension group （P<0.05）, but the changes of ABI and IMT thickening rate were not obvious in the non-As hypertension group （P>0.05）. There was no obvious correlation between baPWV and ABI in the control group and the non-As hypertension group, but there was obviously negative correlation between baPWV and ABI in the As hypertension group （r＝-0.718，P<0.05）.Conclusions The baPWV and ABI can more accurately reflect vascular structure and function changes, and be obviously correlated with the As degree. They are helpful to the early diagnosis of As lesion for patients with hypertension.

Abstract:Aim To analyze the relation of serum sodium level with long-term prognosis in patients with heart failure and preserved ejection fraction.Methods We enrolled 562 consecutive chronic heart failure patients, who were divided into 3 groups according to serum sodium concentration on admission:＜135 mmol/L（hyponatremia group, n105,11.4%）, ＞145 mmol/L（hypernatremia group, n37, 4.0%）and 135 -145 mmol/L（normonatremia group, n783,84.6%）. The primary end point was all-cause mortality. Cox proportional-hazards regression modeling was used to evaluate the relation of serum sodium level to long-term outcome in patients with heart failure and preserved ejection fraction.Results Hyponatremia group patients were older, with more men, higher NYHA status, and faster heart rate, but lower systolic and diastolic blood pressure than other groups. The percentage of hypertension was higher in hypernatremia and normonatremia group. Hyponatremia group patients had lower red blood cells, hemoglobin, albumin, pre-albumin, cholesterol and chlorine, but higher end-systolic volume, serum creatinine, and urea nitrogen. During the median 3.7-year follow-up, there were 135 deaths （24.0%） for all causes, 30 in hyponatremia group （54.5%）, 2 in hypernatremia group （9.1%）, and 103 in normonatremia group （21.2%）. On multivariate COX regression analysis, hyponatremia group had the lowest survival （HR 2.158, 95% CI 1.237-3.766；P0.007） hypernatremia and normonatremia group had the similar survival.Conclusion In patients with heart failure and preserved ejection fraction, hyponatremia is a powerful predictor of long-term mortality, and hypernatremia and normonatremia have the similar survival.

Abstract:Aim To study the effects of two different dosages of atorvastatin on carotid artery plaque using color dopller ultrasound.Methods Newly diagnosed stable angina pectoris patients （n123） with hyperlipidemia and carotid atherosclerotic plaques were randomized to groups of 10 mg/d （n60） or 40 mg/d （n60） atorvastatin for 6 months. Carotid intima-media thickness （CIMT）, carotid artery pulsation index （CAPI）, and carotid artery resistance index （CARI） were compared.Results 10 mg/d and 40 mg/d atorvastatin reduced significantly CIMT and increased high density lipoprotein cholesterol （HDLC） versus baseline （P<0.05）. CAPI and CARI increased in 10 mg/d atorvastatin group, respectively. CAPI, CARI, low density lipoprotein cholesterol （LDLC） and high sensitivity c-reactive protein （hs-CRP） reduced in the 40 mg/d atorvastatin group.Conclusion 40 mg/d atorvastatin treatment can delay the progroression of carotid plaque, and may even reverse the carotid artery plaque.

Abstract:Aim To observe the clinical efficacy and the safty of ticagrelor in patients with clopidogrel resistance.Methods A total of 136 patients with clopidogrel resistance after coronary intervention in the Department of Cardiology from February 2014-December 2014 of our hospital were enrolled in this study, the subjects were divided into ticagrelor group and clopidogrel group according to a randomized controlled principle, 68 cases in each group. Patients with clopidogrel resistance received ticagrelor treatment （90 mg, twice daily） or clopidogrel treatment （150 mg daily）. After the treatment for 3 days patients with thromboelastography were reviewed, to evaluate platelet inhibition rate. Following up six months, observed major adverse cardiovascular events （MACE） and bleeding events were observed.Results After the treatment for 3 days, the inhition ratio against adenosine diphosphate （ADP） in patients with clopidogrel resistance in ticagrelor group was signifycantly higher than in the clopidogrel group, MA_ADP lower than clopidogrel group, the difference was statistically significant （P<0.05）. The incidence of adverse events in the two groups showed no significant difference （P>0.05）. There were no serious bleeding events and cardiovascular deaths during the follow-up. Clopidogrel group had 1 case of stent thrombosis, 1 case of nonfatal myocardial infarction.Conclusions Ticagrelor appliea in patients with clopidogrel resistance has rapid onset and good anti-platelet effect, little serious complications, and the same security effect as clopidogrel, it is worth in clinical practice.

Abstract:Aim To study the blood lipid level of Zhengzhou 10636 government staff so as to provide evidence for lipid preventing.Methods According to the standard of 2007 “Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults”, the lipid level of Zhengzhou 10636 government staff was observed in all age groups.Results The level of total cholesterol （TC） was 4.85±0.93 mmol/L, low density lipoprotein cholesterol （LDLC） was 2.92±0.73 mmol/L, high density lipoprotein cholesterol（HDLC） was 1.34±0.28 mmol/L, and the median of triglyceride （TG） was 1.3（0.94～1.89） mmol/L. The total detection rate of dyslipidemia was 29.7%, and hypercholesterolemia, high blood LDLC, low blood HDLC, hypertriglyceridemia detection rates separately were 7.6%, 5.0%, 10.6%, 16.4%. The levels of TC, LDLC and the detection rate of high blood LDLC in male group of the age 30～39, 40～49 were higher than women of the same age（P<0.001）. But after age 50, TC, LDLC levels of the women in each age group increased significantly, and was higher than that of men, and hypercholesterolemia detection rate of women after the age of 50 higher than men（P<0.001）.Conclusions Blood lipid control should be focused on the middle-aged men and postmenopausal women, at the same time to strengthen young people's awareness of dyslipidemia.

Abstract:Atherosclerosis is the primary cause of cardiovascular and cerebrovascular diseases. Anti-inflammatory therapies hold great promise in cardiovascular prevention and several novel anti-inflammatory drugs have reached clinical development stage. In recent years, the study found that defective inflammation resolution is also important in deciphering the complex process of atherosclerosis progression. Here, this article summarizes the critical aspects of defective inflammation resolution and its influence on Atherosclerosis plaque formation, deeply discusses the efferocytosis of apoptotic macrophages and how it may go awry in advanced atheroma. In addition, this article combines with the mechanism of defective inflammation resolution, discusses the intervention of Traditional Chinese Medicine in inflammation resolution potential targets, in order to seek both anti-inflammatory and pro-inflammatory resolution atherosclerosis drugs and provide scientific and theoretical basis.

Abstract:Atherosclerosis （As） is an important pathological basis of coronary heart disease, cerebral apoplexy disease. In addition to the disorder of lipid metabolism, vascular endothelial injury, oxidative stress and risk factors, many researchers have approved that inflammatory signaling pathway as new risk factors mediated through the formation process of As. Traditional Chinese medicine because of its wide effect, small toxic and side effect, is widely used in the prevention and treatment of As. In this paper, we summarized the action mechanism of inflammatory signaling pathways in As and progress of anti As mechanism of traditional Chinese medicine through intervention in inflammatory signal pathway.

Abstract:The research on the development of atherosclerosis has been recognized as the hot and key point in medical research of China. Focusing on the model and the pathogenesis of atherosclerosis, Chinese researchers executed mass studies in the recent three years, like apoptosis and autophagy, oxidative stress, vascular smooth muscle cell proliferation, vascular inflammation, the function of lipoprotein, non-coding RNA gene polymorphism and epidemiological studies of atherosclerosis, and other aspects that could induce atherosclerosis. What’s more, the investigations on apoptosis and autophagy, epigenetic mechanisms, signal pathway, microRNA, LncRNA, PCSK9 and the application of apolipoprotein mimetic peptide have been the tendency in the cure of atherosclerosis. Chinese researchers have provided several new theories on preventing and curing atherosclerosis, however, a certain gap is still existed between Chinese and international researches.