Abstract:Aim To investigate the role of vascular smooth muscle cell phenotype transformation in carotid artery remodeling of Wistar rats fed by high salt diet, and the intervention of telmisartan. Methods The male Wistar rats were randomly divided into control group (0.5%NaCl feed), model group (4%NaCl feed), telmisartan group (4%NaCl and telmisartan 5 mg/(kg·day) feed). After 24 weeks, changes of morphology and structure of carotid artery were investigated by HE staining and Masson staining. The mRNA and protein levels of α-smooth muscle actin (α-SMA), smooth muscle 22α (SM22α) and osteopontin (OPN) were analyzed by quantitative real-time PCR and immunohistochemical staining. Results Compared with the control group, the blood pressure, media thickness, cross-sectional area, collagen volume fraction, and proliferating cell nuclear antigen (PCNA) positive cells were elevated in the model group. At the same time, the model group showed an increase in the mRNA and protein levels of α-SMA, SM22α, and a decrease of OPN. The telmisartan reduced the blood pressure, media thickness, cross-sectional area, collagen volume fraction, and the expression of PCNA and OPN, compared with the model group. Moreover, the mRNA and protein levels of α-SMA, SM22α were upregulated by telmisartan. Conclusions The 4% high salt diet can cause carotid artery remodeling and elevated-blood pressure in Wistar rats. The vascular smooth muscle phenotype transformation might be involved in the mechanism of carotid artery remodeling induced by high salt. Telmisartan can prevent artery remodeling partially via regulating vascular smooth muscle cell phenotypic transformation.

Abstract:Aim The effects of ghrelin on RAW264.7 derived foam cells migration and its associated mechanisms were investigated. Methods The detection of total cholesterol (TC), free cholesterol (FC), cholesterol ester (CE) and lipid droplets were performed by cholesterol oxides method and oil red O staining, respectively. The effects of ghrelin on RAW264.7 derived foam cells migration were detected by transwell chamber assay, the expression of Akt, p-Akt, cleaved Caspase-3 were semi-quantified by Western blot, the distribution of p-Akt and cleaved Caspase-3 in cells was qualitatively analyzed with fluorescent staining. The dissociation and polymerization of cell cytoskeleton was observed with F-actin fluorescence probe. Results 10-7 mol/L ghrelin could promote the migration of RAW264.7 derived foam cells, which was reversed by LY294002. Western blot analysis showed that 10-7 mol/L ghrelin could significantly increase the expression of p-Akt and reduce the expression of cleaved Caspase-3 (P＜0.05) in RAW264.7 derived foam cells. What’s more, it could improve the ability of RAW264.7 migration obviously (P＜0.05). Interestingly, these processes above can be reversed by LY294002 treatment. Fluorescent analysis demonstrated that there was an obvious expression of Akt in RAW264.7 cells. The treatment of ghrelin could upregulate its expression, while LY294002 treatment downregulated the expression. Conclusion Ghrelin could promote the migration of RAW264.7 derived foam cells, which may be related to the activation of the PI3K/Akt signal pathway.

Abstract:Aim To investigate the effect of different concentration of serum amyloid P component (SAP) on inflammation and oxidative stress and its probable mechanism. Methods RAW264.7 cells were divided into control and SAP group (1.25 mg/L, 2.5 mg/L, 5 mg/L) with different concentrations of SAP co-culturing for 24 hours. Expression of intercellular adhesion molecule 1 (ICAM-1) and Fc gamma receptor (FcγR) were measured by flow cytometry. ELISA and RT-PCR were used to measure inflammatory factors, IL-1β and TNF-α, ICAM-1 and reactive nitric species, nitric oxide (NO). Expression of protein (Spleen tyrosine kinase, Syk, extracellular signal-regulated kinase, ERK1/2 and pERK1/2) related to information was detected by Western blot. Results RAW 264.7 cells were co-cultured with different concentrations of SAP for 24 hours. Secretions of inflammatory factors, IL-1β and TNF-α (P＜0.05), ICAM-1 and NO were significantly increased in SAP groups. However, expressions of FcγR and pERK1/2 were not affected by the treatment of SAP. For the key protein in downstream pathways of FcγR, Syk was dose-dependent increased and downstream pathways was activated. Conclusion SAP increased expression of Syk, promoted secretion of inflammatory factors and oxidative stress after combined with Fcγ receptors.

Abstract:Aim To explore whether warfarin promotes calcification of rat vascular smooth muscle cells (VSMC) through the bone morphogenetic protein (BMP) signaling pathway. Methods Vascular smooth muscle cells were obtained from rat aortic, and identified by immunocytochemistry, then randomly divided into control group, high phosphorus group, warfarin (10 μmol/L) group, warfarin (10 μmol/L)＋vitamin K (10 μmol/L) group. Calcification staining, calcium content and alkaline phosphatase (ALP) activity were measured, the expression of Runx2 protein was detected by Western blot and the expression of BMP-2, Smad1, Runx2 mRNA was detected by RT-PCR. Results The results of alizarin red stain were shown that the number of calcified nodules in the warfarin group was significantly higher than that in the control and high phosphorus group (P＜0.05). The results of calcium content were in line with that of alizarin red stain. The ALP activity in the warfarin group was significantly higher than that in the control and high phosphorus group (P＜0.05). The results of RT-PCR and Western blot were shown that the expression level of Runx2, BMP-2 and Smad1 in the warfarin group was significantly higher than that in the control and high phosphorus group (P＜0.05). However, the calcification content, ALP activity and the expression level of BMP-2, Smad1 and Runx2 in the warfarin＋vitamin K group were significantly lower than those in the warfarin group (P＜0.05). Conclusion The BMP pathway was involved in warfarin-induced vascular calcification of rat vascular smooth muscle cells, which may be achieved by promoting the transdifferentiation of vascular smooth muscle cells.

Abstract:Aim To observe the expression changes of intermediate conductance calcium-activated potassium channel (KCa3.1) and large conductance calcium-activated potassium channel (KCa1.1) in rat thoracic aorta smooth muscle cells induced by high phosphorus in alkaline environment; To explore the relationship between the KCa and the phenotype transformation of rat thoracic aorta smooth muscle cells. Methods Tissue block adherence method was used to culture primary rat aortic smooth muscle cells. Vascular smooth muscle cell (VSMC) calcification model was prepared with 10 mmol/L β-glycerol sodium phosphate. PH value of culture medium was regulated by using HCl and NaHCO₃. Then the cells were divided into 5 groups:normal pH 7.4 group, high phosphorus pH 7.4 group, high phosphorus pH 7.7 group, high phosphorus pH 8.0 group, TRAM-34 intervention group, and cultured for 4 days. The expressions of KCa3.1, KCa1.1α, KCa1.1β, runt-related transcription factor 2 (Runx2) and smooth muscle 22 α (SM22α) were detected by reverse transcription polymerase chain reaction (RT-PCR) in each group cells. Results Compared with normal pH 7.4 group, the expression of Runx2 was increased in high phosphorus groups, and increased with the increase of pH (P<0.05); the expression of SM22α was reduced in high phosphorus groups, and reduced with the increase of pH (P<0.05). Compared with normal pH 7.4 group, the expression of KCa3.1 was increased and the expression of KCa1.1α was reduced in high phosphorus pH 7.4 group (P<0.05). In the high phosphorus groups, the expressions of KCa3.1 and KCa1.1α were increased with the increase of pH (P<0.05). In the same group, the expression of KCa3.1 was more than KCa1.1α (P<0.05). There was no significant difference in KCa1.1β expression among 3 high phosphorus groups (P>0.05). Compared with high phosphorus pH 8.0 group, the expression of Runx2 was decreased and the expression of SM22α added in TRAM-34 intervention group (P<0.05). Correlation analysis showed that KCa3.1 expression was positively correlated with Runx2 expression (r＝0.945, P<0.01) and was negatively correlated with SM22α expression (r＝－0.926, P<0.01). KCa1.1α expression was negatively correlated with Runx2 expression (r＝－0.746, P＝0.029) and was positively correlated with SM22α expression (r＝0.971, P＝0.002) in normal pH 7.4 group and high phosphorus pH 7.4 group. KCa1.1α expression was positively correlated with Runx2 expression (r＝0.805, P＝0.002) and was negatively correlated with SM22α expression (r＝－0.806, P＝0.005) in high phosphorus pH 7.7 group and high phosphorus pH 8.0 group. The expression of KCa1.1β was not correlated with the expression of Runx2 and SM22α (r＝0.414, P＝0.356; r＝－0.155, P＝0.714). Conclusion The expression of calcium-activated potassium channel in smooth muscle cells is involved in the phenotypic transformation of rat thoracic aorta smooth muscle cells induced by high phosphorus in alkaline environment.

Abstract:Aim To investigate the effect of maternal perinatal high-salt diet on dimethylarginine dimethylamino-hydrolase 2 (DDAH2)/asymmetric dimethylarginine (ADMA)/endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) pathway of the mesenteric artery in the male offspring rats. Methods The rats were divided into 2 groups:normal-salt diet (NSD) group and high-salt diet (HSD) group, and fed respectively with normal-salt diet (1%NaCl) and high-salt diet (8%NaCl) during perinatal period. After delivery, the male offspring rats were fed with the same diet for 16 weeks. Blood pressure, mesenteric artery endothelial-dependent diastolic function, NO content, eNOS activity and ADMA content in plasma and mesenteric artery, DDAH2 activity and protein expression of DDAH1 and DDAH2 in mesenteric artery were detected by various methods. Results The systolic blood pressure (SBP) in HSD group was significantly higher than that in NSD group (P<0.01). The endothelium-dependent tension of mesenteric artery in HSD group was lower than that in NSD group (P<0.01). After incubation with ADMA, the blood vessel tension was significantly decreased in NSD group, while no significant change was found in HSD group. Compared with the NSD group, NO content was decreased (P<0.05), eNOS activity was decreased (P<0.01), ADMA content was increased (P<0.05) in plasma in HSD group, and NO content was decreased (P<0.01), eNOS activity was decreased (P<0.01), ADMA content was increased (P<0.05) on mesenteric artery in HSD group. In HSD group, DDAH2 activity and protein expression were decreased (P<0.01), but DDAH1 protein expression was not changed significantly. In HSD group, correlation analysis of mesenteric arterial indexes showed that eNOS activity was positively correlated with NO content, ADMA content was negatively correlated with eNOS activity, DDAH2 activity and DDAH2 protein expression were negatively correlated with ADMA content. Conclusion The high-salt diet in the maternal perinatal period results in the increase of SBP and the endothelial-dependent diastolic dysfunction on mesenteric arteries in male offspring rats, which are related to the decrease of DDAH2 activity and the disorder of DDAH2/ADMA/eNOS/NO pathway in mesenteric arteries.

Abstract:Aim To observe the anti-senescence effects of aspirin on activity of dimethylarginine dimethylaminohydrolase (DDAH)-asymmetric dimethylarginine (ADMA) system and caveolin-1 protein expression in human umbilical vein endothelial cells (HUVEC) exposed to high glucose condition and explore the mechanism of aspirin of anti-senescence. Methods The human umbilical vein endothelial cells (HUVEC) were cultured in Dulbecco's modified Eagle's medium (DMEM) containing 5.5 mmol/L glucose as normal level, 33 mmol/L glucose as high glucose, aspirin (0.01～1 mmol/L) with high glucose and 300 μmol/L L-NAME was added to the culture medium when needed for 48 hours. The activity of DDAH were reflected by ADMA concentration determined by high-performance liquid chromatography. The level of intracellular reactive oxygen species (ROS) was monitored by flow cytometry. Caveolin-1 protein expressions were analyzed by Western blot. Results After the endothelial cells were treated with high glucose concentration for 48 hours, the number of SA-β-gal positive cells, the level of ROS, ADMA and caveolin-1 protein were increased significantly. While, the activity of DDAH was decreased dramatically(P<0.05). All these changes were reversed by aspirin (0.01～1 mmol/L) remarkably in a dose-dependent manner (P<0.05). However, all the effects of aspirin on senescence were completely inhibited by L-NAME, the NOS inhibitor(P<0.05). Conclusion The anti-senescent effects of aspirin were fulfilled by inhibiting caveolin-1 protein expression and regulating the activity of DDAH-ADMA system.

Abstract:Aim To explore the effects of NOD1/receptor-interacting protein 2(RIP2) signal pathway on macrophage inflammatory activation and phenotype by human monocytic cell line THP-1. Methods Human THP-1 cells were differentiated into macrophages by addition of 160 nmol/l phorbol 12-myristate 13-acetate (PMA) for 24 h. Macrophages were incubated with different concentrations of ox-LDL(0,5, 50 mg/L) for 24 h. The expression of NOD1 and RIP2 was detected by RT-PCR and Western blot. ELISA was used to detect the secretion of monocyte chemotactic protein 1 (MCP-1) and macrophage migration inhibition factor (MIF). FACS was used to detect membrane molecule CDl6/CD68. Results ox-LDL could up-regulate the expression of NOD1/RIP2 signal pathway as a dose-dependent manner in THP-1 derived macrophages. The expression of NOD1, RIP2 mRNA and protein was up-regulated followed the increasing concentrations of ox-LDL. Activation of NOD1 /RIP2 signaling pathway increased the expression of MCP-1 and MIF from the cell culture supernatants. With the increasing concentrations of ox-LDL, the secretion of MCP-1 and MIF increased(P<0.05). The activation of NOD1/RIP2 signaling pathway could change the expression of membrane molecule CD16/CD68. With the different ox-LDL concentrations, the mean fluorescence intensity of CD16/CD68 varied. 50 mg/L group could significantly reduce the expression of CD16/CD68(P<0.01). Conclusion ox-LDL can up-regulate the expression of NOD1/RIP2 signal pathway in a dose-dependent manner in macrophages. NOD1/RIP2 signal pathway enables the macrophage inflammatory activation and polarity switch, which may be the main mechanism in the initiation and progression of atherosclerosis.

Abstract:Aim To analyze the risk factors of new diagnosed mild or moderate nonalcoholic fatty liver disease (NAFLD), and investigate the vascular damage and endothelial function in patients with NAFLD. Methods 202 new diagnosed patients with mild or moderate NAFLD and 91 healthy controls were selected in the Health Center of the Eighth Hospital of Changsha. Intima-media thickness (IMT) of carotid artery, flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD) in brachial artery were measured by high-resolution ultrasound. The clinical and biochemical characteristics were analyzed between the two groups. Results (1)Compared with the controls, body mass index, waist circumference, hip circumference, waist-hip ratio, systolic blood pressure, diastolic blood pressure, fasting insulin, fasting plasma glucose, low density lipoprotein, total cholesterol, triglycerides, alanine aminotransferase(ALT), aspartate aminotransferase(AST), uric acid, high sensitivity C-reactive protein, HOMA-insulin resistance index were higher, and high density lipoprotein was lower in NAFLD group(P<0.01). (2)Multi-factor logistic regression analysis demonstrated that NAFLD was independently correlated with HOMA-insulin resistance index, high sensitivity C-reactive protein, ALT(OR=2.5,1.3,1.054, P<0.05). (3) Compared with the controls, NAFLD group had higher IMT(0.92(0.0,1.02) vs 0.87(0.4,0.99)), lower FMD (4.7%(2.2%,6.8%) vs 5.2%(2.4%,7.7%)) and NMD (18.5%(12.2%,25.3%) vs 20.5%(12.2%,28.7%)), but this differences had no statistical significance. The differences of IMT, FMD, NMD between the mild and moderate NAFLD groups had also no statistical significance. Bivariate correlation analysis between IMT, FND, NMD and NAFLD had no statistical significance. Conclusion HOMA-insulin resistance index, high sensitivity C-reactive protein, body mass index are independent risk factors for NAFLD. There was no significant differences in vascular damage between patients with mild or moderate NAFLD and healthers, the exact association between vascular damage and NAFLD need further research.

Abstract:Aim To detect the levels of plasma oxidized low density lipoprotein (ox-LDL) and platelet aggregation in patients with acute coronary syndrome (ACS), and explore the effects of ox-LDL on the levels of platelet aggregation in patients with ACS. Methods A total of 158 patients with coronary heart disease (CHD) diagnosed by coronary angiography were enrolled in this study, including 48 patients with stable angina (SA), 59 patients with unstable angina (UA) and 51 patients with acute myocardial infarction (AMI). In addition, 60 hospital patients, chest pain without coronary artery stenosis, served as a control group. The levels of plasma ox-LDL were determined by ELISA, the levels of platelet aggregation were detected by turbidimetric aggregation monitoring device. Results Compared with control group, the levels of plasma ox-LDL and platelet aggregation were significantly increased in patients with UA and AMI, and there was no obvious change between control group and SA group, UA and AMI groups. In addition, the levels of plasma ox-LDL were positively correlated with the levels of platelet aggregation. Moreover, in vitro, ox-LDL could markedly promote ADP-induced platelet aggregation in patients with ACS. Conclusions Increased levels of plasma ox-LDL were associated with elevated levels of platelet aggregation in patients with ACS. Increased levels of plasma ox-LDL played a key factor role in the formation of atherothrombosis in patients with ACS, therefore, it was crucially important to detect the levels of ox-LDL in patients with ACS.

Abstract:Aim By testing cholesterol absorption and synthesis markers of hyperlipidemia patients reveals cholesterol metabolism traits and correlation between the blood lipids and other risk factors. Methods 53 hyperlipidemia patients and 50 healthy persons were enlisted to detect liver and kidney function, serum total cholesterol (TC), low density lipoprotein cholesterol (LDLC), triglyceride (TG), fasting plasma glucose (FPG) and other indicators, and serum markers of cholesterol synthesis and absorption were determined by gas chromatogram. Results Squalene, lathosterol synthesis rate in patients with hyperlipidemia were higher than those in healthy control group (P＜0.05). Stigmasterol absorption markers were higher than those in healthy control group (P＜0.05). Multiple linear stepwise regression analysis showed the independent influencing factors of TG were LDLC and campesterol, the independent influencing factors of TG were LDLC and desmosterol, independent factors of TC and TG in health control group were LDLC and lathosterol. Conclusions Cholesterol metabolism markers in patients with hyperlipidemia were significantly higher than those in healthy control group in squalene, lathosterol, and the decreased rate of stigmasterol cholesterol absorption that results in increasing absorption of cholesterol was lower than healthy control group. The independent risk factors affecting TC and TG of hyperlipidemia group were cholesterol synthesis (dehydrogenation cholesterol) and cholesterol absorption markers (campesterol) except LDLC.

Abstract:Aim To investigate the relationship between serum oxidized low density lipoprotein (ox-LDL), monocyte chemotactic protein-1 (MCP-1) and carotid atherosclerosis (CAS) in patients with cerebral infarction. Methods112 cases of acute anterior circulation cerebral infarction were selected as the cerebral infarction group, 49 cases of healthy persons were as control group, and all of them underwent carotid artery ultrasound examination. According to the carotid intima-media thickness (IMT), cerebral infarction group was divided into IMT normal group, IMT thickening group and plaque group. According to the plaque echo characteristics, plaque group was divided into strong echo plaque group, mixed echo plaque group and low echo plaque group. Serum levels of ox-LDL and MCP-1 were compared between cerebral infarction group and control group, and among different types of cerebral infarction subgroups. Results The serum levels of ox-LDL and MCP-1 in the cerebral infarction group were higher than those in the control group (P＜0.05). The serum levels of ox-LDL and MCP-1 in the plaque group were higher than those in the IMT normal group and the IMT thickening group (P＜0.05). The serum levels of ox-LDL and MCP-1 in the low echo plaque group were higher than those in the strong echo plaque group and the mixed echo plaque group (P＜0.05). Conclusion In patients with cerebral infarction, the higher the serum levels of ox-LDL and MCP-1, the higher the degree of CAS, the higher the incidence of plaque, and the majority of low echo plaque.

Abstract:Aim To evaluate the correlation between left ventricular structure and function parameters and degree of coronary stenosis by using cine magnetic resonance imaging (MRI). Methods 62 cases suspected with coronary heart disease from 2012 to 2013 underwent cine MRI examination to evaluate left ventricular structure and function parameters and degree of coronary stenosis. The stenosis segments of each branch coronary artery were evaluated according to modified Gensini score (GS). All patients were divided into four groups:GS＜5 scores group (10 cases), 5 scores≤GS＜25 scores group (13 cases), 25 scores≤GS＜60 scores group (20 cases) and GS≥60 scores group (19 cases). The correlation was analyzed betwween left ventricular structure and function parameters and GS score. Results The differences of cardiac output (CO) and stroke volume (SV) were not significant among different groups (F＝6.8,5.641, P＞0.05). Left ventricular end systolic volume (LVESV), left ventricular end diastolic volume (LVEDV), left ventricular ejection fraction (LVEF) and myocardial mass (MM) were significantly different among different groups (F＝23.2,1.1,2.5,5.621, P＜0.01). There was no correlation between CO, SV and GS score (P＞0.05). LVEF was negatively correlated with GS score, whereas LVESV, LVEDV, MM were positively correlated with GS score (P＜0.05). The segments deviated from normal values of wall thickness of end systole (WTES), wall thickness of end diastole (WTED), wall thickening % (WT%) and wall motion (WM) were most in the GS≥60 scores group; Deviation segments reduced gradually along with 25 scores≤GS＜60 scores group, 5 scores≤GS＜25 scores group and GS＜5 scores group; The differences were significant among different groups. WTES, WTED, WT% and WM were positively correlated with GS score. Conclusions Left ventricular function becomes worse with the increase of the GS score. Cine MRI can effectively evaluate the myocardial ischemia, and thus, it can help early diagnosis of coronary heart disease.

Abstract:Aim To investigate the correlations between carotid plaque types, non-HDLC/HDLC and non-HDLC in patients with acute coronary syndrome (ACS). Methods This study consists of 95 patients with ACS, 30 patients with stable angina pectoris (SAP), and 49 healthy individuals who have no history of heart diseases serving as controls. All the selected cases underwent ultrasound examination of their carotid artery to diagnose carotid plaque types. The carotid plaques were classified into three types:soft plaque, fibrous plaque and calcified plaque. Their serum total cholesterol (TC), high density lipoprotein cholesterol (HDLC), triglyceride (TG), and low density lipoprotein cholesterol (LDLC) levels were measured and recorded, and the non-HDLC/HDLC ratio was calculated. Results The results showed that, non-HDLC/HDLC ratio was higher in ACS patients (P＜0.05 or P＜0.01) as compared to the SAP patients and the control subjects. The HDLC level was observed to be lower in ACS patients compared with the controls (P＜0.05). An increased level of non-HDLC was seen in ACS patients compared to the SAP patients (P＜0.05).The prevalence of carotid plaque within the ACS patients was significantly higher than that of the control subjects (P＜0.001). The prevalence of soft plaque was significantly higher (P＜0.05) and the prevalence of fibrous plaque was significantly lower (P＜0.05 or P＜0.01) in ACS patients than in SAP patients and control subjects. It was observed that the level of non-HDLC and non-HDLC/HDLC ratio were high in all the three types of carotid plaque, but the non-HDLC (P＜0.01) level and non-HDLC/HDLC ratio (P＜0.05) in the soft plaque group was significantly higher than in calcified plaque group. The receiver operating characteristics (ROC) curve analysis was used to calculate the area under the curve (AUC) for non-HDLC and non-HDLC/HDLC in ACS patients with soft plaque, which showed that AUC of non-HDLC was 0.722±0.060 (95%CI was 0.604～0.841, P＜0.01) and AUC of non-HDLC/HDLC was 0.669±0.062 (95%CI was 0.548～0.790, P＜0.01), respectively. Conclusion Our findings support that the higher level of non-HDLC/HDLC ratio is a risk factor for soft plaque in patients with ACS. Non-HDLC and non-HDLC/HDLC ratio can be considered as predictors for soft plaque in patients with ACS.

Abstract:Aim To discuss the influence of reteplase thrombolytic therapy and emergency PCI treatment on ventricular remodeling and left ventricular function after acute myocardial infarction within 3 hours. Methods 98 patients were randomly divided into reteplase thrombolytic therapy group and emergency PCI treatment group. Compare cardiac function indexes of the two groups, such as NT-ProBNP, ejection fraction, end systolic volume index, end diastolic volume index, ventricular wall motion score index. Results There were no significant differences between the two groups in NT-ProBNP, ejection fraction, end systolic volume index, end diastolic volume index and ventricular wall motion score index (P＞0.05). Conclusion These two treatments have the same effect on the left ventricular function in acute myocardial infarction within 3 hours. Both of them are effective reperfusion therapies. They can reduce and delay ventricular remodeling, and reduce the incidence of heart failure.

Abstract:Aim To evaluate the lipid profile in non-treated patients with coronary artery disease (CAD); To explore the prediction factors of CAD. Methods 1772 patients with clinically suspected CAD and without use of lipid-regulating drugs were enrolled, and undergone by coronary angiography. 1057 cases were diagnosed as CAD, and 715 cases were without CAD. Blood lipid profiles of the two groups were analyzed and compared. Correlation between blood lipid levels and CAD was analyzed. Results The blood lipid profiles in patients with CAD were as follows:triglyceride 1.78 mmol/L (1.29-2.43 mmol/L), total cholesterol (TC) 4.92±0.99 mmol/L, high density lipoprotein cholesterol (HDLC) 1.09±0.29 mmol/L, low density lipoprotein cholesterol (LDLC) 3.22±0.91 mmol/L. LDLC and non-HDLC were able to meet the standards (LDLC＜1.81 mmol/L and non-HDLC＜2.59 mmol/L) in only 2.46% patients with CAD. In 50-59 years, 60-69 years, ≥70 years subgroups, the levels of TC, HDLC, apolipoprotein A1 (ApoA1) and ApoB in male patients were significantly lower than that in female patients (all P＜0.05). ApoB/ApoA1 was the strongest predictor of CAD. Conclusion Blood lipids levels are increased in CAD patients without use of lipid-regulating drugs, most of which are mild or moderate dyslipidemia, and standard-reaching rate of blood lipids is low. The degree of abnormal blood lipids is more serious in women. Correlation between non-HDLC, ApoB, LDLC/HDLC, ApoB/ApoA1 and CAD is good, which can predict the risk of CAD.

Abstract:Reverse cholesterol transport (RCT) is an important mechanism to remove cholesterol, and it has important significance to maintain cholesterol homeostasis and prevent atherosclerosis. ATP-binding cassette transporter A1 (ABCA1) is the key factor of RCT, the expression of ABCA1 is controlled by many factors of transcriptional level and post-transcriptional level. The post-transcriptional level of the expression of ABCA1 mediated by microRNA, is attached importance. According to the recent researches, kinds of microRNAs have regulated the ABCA1 expression directly by treating the ABCA1 as target gene, at the same time, they also have found some microRNAs take effects indirectly by regulating the transcription factor of the ABCA1 gene. For example, liver X receptor α (LXRα), peroxisome proliferator activated receptor γ (PPARγ), retinoid X receptor α (RXRα) are regulating ABCA1 expression, so as to affect cholesterol efflux, these microRNAs include miR-33a/b, miR-19b, miR-27a/b, miR-302, miR-758, miR-106b and so on. This article mainly reviews various known microRNAs influence on ABCA1 expression.

Abstract:Atherosclerosis is a fairly common disease associated with heart and brain blood vessels, posing serious cardiovascular complications. Western medicine is the main means of treatment of atherosclerosis. In recent years, with the experimental and clinical research on atherosclerosis, the traditional Chinese medicine has made remarkable progress in the treatment of arteriosclerosis, but the therapeutic effect of atherosclerosis is still not satisfied. In this review, we will explore the relationship between the pathogenesis of traditional Chinese medicine and western medicine in atherosclerosis, and try to provide reference for atherosclerosis therapy with integrated Chinese and Western medicine.

Abstract:Bone morphogenetic proteins-4 (BMP-4), a member of the transforming growth factor β (TGF-β) superfamily, is a multi-functional growth factor that plays key roles in embryonic development, angiogenesis, cell proliferation and differentiation, skeletal formation, ectopic osteogenesis, fracture repair, and et al. Vascular calcification(VC) is considered as an actively regulated and complex process, similar to osteogenesis. The transdifferentiation process of vascular smooth muscle cells(VSMC) to the osteogenic phenotype plays a crucial role in the formation of VC. In recent years, researches have shown that BMP-4 may be implicated in the formation and progress of VC, but the specific mechanism has not yet been elucidated. The relationship between BMP-4 and VC are reviewed in this paper.

Abstract:Metabolomics is an emerging system biology following the genomics and proteomics, which has attracted extensive interest in the field of disease study. ¹H-NMR as an important technology of metabolomics, is widely used because of its high speciality and sensitivity, simple procedure and lossless to the samples. Cardiovascular disease is an important part of human disease, and this article reviewed the status quo of its advances in cardiovascular diseases.

Abstract:With the development of molecular biology technology in recent years, cardiovascular disease research entered the era of genetic testing. An increasing number of studies shows that, lncRNA not only has close relationship with cardiovascular disease, but also plays a key role in cardiovascular disease of the regulation mechanism. This review focuses on the association between lncRNA and cardiovascular disease.