Abstract:Aim To investigate the changes of autophagy of the common carotid atherosclerosis (As) at the different stages in apolipoprotein E gene knockout (ApoE－/－) mice. Methods 6-weeks-old male ApoE－/－ mice (n=40) were randomly divided into two groups and fed with common adaptability diet for 2 weeks. The mice of the control group (n=10) received a sham operation and the common diet for another 8 weeks. While the model mice (n=30) received a right common carotid artery cannulation and then were randomly subdivided into three groups (the 2 weeks, the 4 weeks and the 8weeks) and fed with the high fat diet separately for 2 weeks, 4 weeks and 8 weeks. The blood samples obtained from femoral arteries were studied via the biochemical analysis. The right common carotid arteries were split out for TEM and histopathological study. Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot were used to detect the relative expression levels of mRNA and protein about ATG5, Beclin1 and LC3-Ⅱ. Results As the operation time prolonged the lipid levels especially TG and LDLC were increased time-dependently. The histopathological analysis results showed that there was a small amount of cells infiltrated in the common carotid artery in the 2 weeks, although the wall was still unspoiled. The vascular wall in the 4 weeks was messy and there was thrombus in the vascular lumen. The thickness of the right common carotid artery in the 8 weeks was higher than the rest and its elastic membranes significantly decreased. The TEM study indicated that the quantity of autophagosomes in the 4 weeks was higher than other groups and its lipid droplets was still higher than the 2 weeks but lower than the 8 weeks. The qRT-PCR and Western blot detection suggested the mRNA and protein expression of ATG5, Beclin1 and LC3-Ⅱ in the 4 weeks was higher than the 2 weeks and the 8 weeks, and the expression in the 8 weeks was also higher than those in the 2 weeks. Conclusion Autophagy was continuously stimulated during As formation, however, the levels of autophagy will decrease after reaching the peak at a time.

Abstract:Aim To investigate the effect of hyaluronic acid (HA) on the expression of interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α (TNF-α) in human aortic vascular smooth muscle cell (HA-VSMC) induced by free fatty acid (FFA). Methods HA-VSMCs were cultured and dealt with different concentrations (0,0, 0,0 μmol/L) of FFA and FFA plus high molecular weight HA (HMW-HA) or low molecular weight HA (LMW-HA) for 4,8 hours. The effects of FFA and FFA plus HA on the survival rate of HA-VSMCs were detected by methyl thiazolyl tetrazolium (MTT) method. Cell proliferation activity was detected by EdU staining. The contents of IL-6, IL-8 and TNF-α in culture supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Real-time fluorescence quantitative PCR and Western blot were used to detect the expression levels of IL-6, IL-8 and TNF-α mRNA and protein. Results(1)FFA showed a concentration-dependent induction to HA-VSMC proliferation in the 400 μmol/L. (2)HMW-HA and LMW-HA both inhibited the proliferation of HA-VSMC induced by FFA, and the inhibitory effect of HMW-HA was stronger than that of LMW-HA. (3)FFA significantly promoted the secretions of HA-VSMC IL-6, IL-8 and TNF-α in a apparent time- and concentration-dependent manner; HA could inhibit the above effect. (4)Real-time fluorescence quantitative PCR and Western blot results showed that the expression levels of IL-6, IL-8, TNF-α mRNA and protein in FFA＋HMW-HA group and FFA＋LMW-HA group were lower than those in FFA group (all P＜0.01), where the FFA＋HMW-HA group was lower than the FFA＋LMW-HA group (P＜0.01). Conclusions (1)FFA can induce the increases of IL-6, IL-8 and TNF-α mRNA and protein expressions in HA-VSMCs. (2)HA can inhibit the expressions of IL-6, IL-8 and TNF-α induced by FFA, and the inhibitory effect of HMW-HA is stronger than that of LMW-HA.

Abstract:Aim To establish valve calcification model , Human heart valve interstitial cells (hVICs) were cultured in vitro and induced by calcification liquid, observing the expression of Notch1 protein , apoptosis in the process of hVICs calcification and revealing the role of Notch1 protein in the relationship between hVICs apoptosis and calcification.Methods hVICs were randomly divided into two groups, the experimental group were treated with calcification induced liquid (beta glycerol phosphoric acid, ascorbic acid, dexamethasone, recombinant type human bone morphogenetic protein 2) to establish the models of calcification, hVICs were stimulated by calcification liquid for 1day, 3days, 5days, 7days ; Control group was cultured with normal culture medium, all hVICs were cultured for 7 days, then detecting the number of calcification nodule ,the expression of BMP-4, Notch1 and the Apoptosis rates of hVICs. Calcification induced cells in experimental group were randomly divided into three groups and cultured in vitro for 3 days, the lipopolysaccharide group (LPS), the Notch1 inhibitor group (γ secretase inhibitor, DAPT), and the control group ( treated with calcification induced liquid). The expression of BMP-4, Notch1, Cysteinyl aspartate specific proteinase 3(Caspase3)were determined.Results The expression of Notch1 protein and cell calcification in experimental group were higher than control group and increased along with the induced days. The rate of cell apoptosis was the highest at the third day, then there was a gradual downward trend. Cell apoptosis and calcification in LPS group were aggravated with the increased expression of Notch1 compared with control group. In DAPT group compared with the control, cell apoptosis and calcification were reduced. Conclusion The relationship between apoptosis and calcification are close, Notch1 protein plays an important role in the relationship between apoptosis and calcification of hVICs.

Abstract:Aim To explore the role of serum S-adenosylmethionine (SAM)/S-adenosylhomo cysteine (SAH) in vascular atherosclerosis B1 repetitive sequence DNA methylation induced by Hcy in ApoE―/― mice. Methods 36 male Apo E―/― mice fed for 4 months were randomly divided into 3 groups:model control group, high methionine group and folic acid＋VitB₁₂ intervention group, 12 mice in each group, and they were respectively fed with different diets. 12 healthy 4-week-old male C57BL/6J mice were taken as normal control group which were fed with normal diet for 15 weeks.The atheromatous plaque were detected by HE staining, the levels of SAM and SAH in the serum were detected by high performance liquid chromatography (HPLC) and the methylation levels of B1 repetitive sequences by methylmion specific PCR (MSP). Results Compared with the normal control group, serum Hcy levels of high methionine group were significantly increased by 2.39 fold (P＜0.01). The arterio-plaque formed in the high methionine group by HE staining. The expression of SAM/SAH increased by 1.68 and 2.75 fold in the model control group and the high methionine group (P＜0.01). Compared with the normal control group, the methylation levels of B1 repetitive sequences significantly decreased 11.8% in the high methionine group (P＜0.05), and had negative correlation with SAM/SAH(r＝－0.3638,P＝0.0210).Conclusion B1 repetitive sequences in ApoE―/― mice had DNA low methylation and it was negatively correlated with SAM/SAH, which suggested that serum SAM/SAH could be used as a biological index to determine vascular As.

Abstract:Aim To observe the relationship between the angiotensin Ⅱ Type 1 receptor autoantibody (AT1-AA) and the local inflammation of plaques in atherosclerotic animal model. Methods AT1-AA positive and negative sera were collected and purified from patients with hypertension complicated with acute coronary syndrome. Atherosclerosis models were established in 30 rabbits with hyperlipidemia induced by balloon injury. The animals were randomly divided into 6 groups:(1)control group; (2)low concentration AT1-AA [20 μg/(kg·d)] injection group (LA group); (3)high concentration AT1-AA [40 μg/(kg·d)] injection group (HA group); (4)losartan [20 mg/(kg·d)] lavage＋high concentration AT1-AA injection group (L＋HA group); (5)simvastatin [4 mg/(kg·d)] lavage＋high concentration AT1-AA injection group (S＋HA group); (6)7aa [1.5 mg/(kg·d)] lavage＋high concentration AT1-AA injection group (7aa＋HA group). Each group was treated differently. The abdominal aortas of rabbits were taken out and stained with HE.Image-Pro Express system was used to measure the percentage of atheromatous plaques in the area of lumen. The expressions of MMP-2 in aortic tissue were detected by western blot. Results The values of total cholesterol and low density lipoprotein cholesterol were obviously increased after four weeks. Excluding the control group, the levels of serum AT1-AA in the 8th and 10th week were significantly higher than those at the beginning in the other groups. In LA group and HA group, the relative plaque areas were 46.99%±13.06% and 66.11%±19.67%, respectively, which were significantly higher than those in control group (27.71%±7.46%), L＋HA group (34.27%±12.38%), S＋HA group (24.03%±8.56%) and 7aa＋HA group (28.54%±12.50%) (all P＜0.05). The expressions of MMP-2 in LA group and HA group were significantly higher than those in other groups (all P＜0.05). Conclusion AT1-AA can accelerate the atheromatous plaque formation in rabbit atherosclerosis model and promote the inflammatory reaction and cells proliferation in local plaque.

Abstract:Aim To investigate the effect of Allicin on foam cell formation and atherosclerosis in ApoE－/－ mice fed with high-fat diet, and to further explore the possible molecular mechanisms. Methods 6-week ApoE－/－ mice were randomly divided into four groups:normal diet, high-fat diet, high-fat diet with low dose of Allicin, high-fat diet with high dose of Allicin. Total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDLC) and high density lipoprotein cholesterol (HDLC) were examined by a commercially available kit. Moreover, atherosclerotic plaque and foam cell formation were analyzed by oil red O, respectively. Further, the expression of SR-A and CD36 and the phosphorylation of JNK and p38 were determined by western blot. Results The level of TC, TG and LDLC in high-fat diet mice were dose-dependently decreased by Allicin(P<0.05). In addition, oil red O staining revealed that Allicin significantly inhibited the increase of atherosclerotic plaque and foam cell formation in high-fat diet mice(P<0.05). Furthermore, administration of Allicin markedly ameliorated high-fat diet induced increase of SR-A and CD36 expression and JNK and p38 phosphorylation in peritoneal macrophages(P<0.05). Conclusion Our findings demonstrate that Allicin ameliorates foam cell formation and atherosclerosis through inhibition of SR-A and CD36 expression and JNK and p38 phosphorylation.

Abstract:Aim To observe the expression of miR-221-3p in ischemic disease of lower extremity. MethodsUsing microarray to screen the different expression of miR-221-3p in arteriosclerosis obliterans(ASO) patients, then real time-PCR was further used to confirm the changes in 55 ASO patients and 54 healthy volunteers. Male SD rats were divided into hind-limb ischemia groups, sham operation group respectively. The laser Doppler imager was performed to evaluate the blood flow at different time points after operation. Then, the rats were sacrificed and the gastrocnemius and plasma were achieved to be further examined after angiography. Results Real-time PCR verified that the level of miR-221-3p was significantly decreased in the plasma, sclerotic samples or gastrocnemius compared with the controls no matter in the ASO patients or SD rat model. Conclusion MiR-221-3p could be a useful biomarker for ASO patients and may contribute to clinical decision making in treatments.

Abstract:Aim To investigate the impact of policosanol combined with atorvastatin on high-density lipoprotein subfractions. Methods A total of 49 consecutively patients with hyperlipidemia were assigned to receive placebo (control group, n=17), atorvastatin 20 mg (n=16) or policosanol 20mg combined with atorvastatin 20 mg (n=16). The baseline clinical characteristics were collected and the HDL lipoprint system was used for lipid subfraction quantification. Results After 8 weeks’ treatment, the reduction of triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC) was significant in both atorvastatin group and policosanol combined with atorvastatin group (P<0.05 or P<0.001, respectively), while the change of high-density lipoprotein cholesterol (HDLC) level had no significant difference (P>0.05). Both in groups of atorvastatin and policosanol combined with atorvastatin, large HDLC subfraction level and large HDLC subfraction percentage significantly increased after treatment (all for P<0.05), while small HDLC subfraction level and small HDLC subfraction percentage markedly reduced. Further analysis showed that the reduction of small HDLC subfraction level and small HDLC subfraction percentage was more marked (P<0.05 for atorvastatin group and P<0.001 for policosanol combined with atorvastatin, respectively) in policosanol combined with atorvastatin group compared to atorvastatin group. Conclusion After treatment with atorvastatin or policosanol combined with atorvastatin, the distribution of HDL subfractions was significantly improved by an increase of large HDL subfraction and a reduction of small HDL subfraction. The reduction of small HDLC subfraction level and percentage was more marked in policosanol combined with atorvastatin group than that in atorvastatin group.

Abstract:Aim To investigate the association between plasma homocysteine (Hcy) and the C677T gene polymorphism of its key metabolic enzyme, methylenetetrahydrofolate reductase (MTHFR), and blood lipid abnormality among hypertensives of Chinese Han population. Methods A total of 312 adult essential hypertensive patients were selected as the study subjects. The average age of the selected patients was 58.25 years old, 178 cases were male, 134 cases were female. The personal information was collected, clinical biochemical indicators were tested, including plasma Hcy, serum lipid, fasting blood glucose (FBG), uric acid (UA) and so on. The C677T gene polymorphism of MTHFR was tested.According to guidelines for prevention and treatment of serum lipid in Chinese adults published in 7,4 cases were elected out as essential hypertension with blood lipid abnormality group and 118 cases as blood lipid normality group, and the blood lipid abnormality group was divided into 4 subgroups:54 cases of hypercholesterolemia group, 53 cases of hypertriglyceridemia group, 59 cases of mixed hyperlipidemia, and 22 cases of hypo high density lipoprotein cholesterolemia group, and subgroup analysis was performed. Results The body mass index (BMI), FBG, and UA of the blood lipid abnormality group were higher than those in the the blood lipid normality group (P＜0.01). There was no significant difference in the MTHFR C677T genotype frequency and allele frequency between blood lipid abnormality group and blood lipid normality group. Subgroup analysis showed that there was no significant difference in the MTHFR C677T genotype frequency and allele frequency among different subgroups, and also no significant difference between subgroups and blood lipid normality group. The level of different blood lipid was not significant among genotypes. The level of Hcy in TT genotype was higher than that in CT and CC genotype (P＜0.05), the level of Hcy was not significant between CT and CC genotype (P＞0.05). Plasma Hcy was negatively correlated with high density lipoprotein cholesterol (HDLC)(r＝－0.116, P＜0.05), but had no correlation with total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDLC) (P＞0.05). After adjusting for age, BMI, UA and FBG, the correlation between Hcy and LDLC disappeared. Logistic regression analysis showed that the correlation between MTHFR C677T gene polymorphisms and blood lipid abnormality was not significant. Conclusions MTHFR C677T polymorphisms was closely related to plasma Hcy, but had no correlation with blood lipid abnormality. The blood lipid abnormality was significantly associated with FBG, plasma UA and BMI, having no correlation with plasma Hcy, but plasma Hcy was negatively correlated with HDLC.

Abstract:Aim To investigate the relationship between carotid stenosis and endothelial progenitor cells (EPC) and the regulation of insulin-like growth factor-1 (IGF-1) on EPC and its mechanism. Methods 35 patients with cerebral infarction and carotid stenosis were enrolled into the carotid stenosis group. At the same time, 11 healthy control subjects were selected as control group. According to the results of cerebral angiography, carotid stenosis group was divided into 3 subgroups: mild stenosis group, middle stenosis group, severe stenosis group. The serum IGF-1 concentration of the study subjects was determined. Mononuclear cells were isolated by density gradient centrifugation and cultured with endothelium growth medium 2 (EGM2), and the double staining method was used to identify EPC. The experiment was divided into 4 groups:untreated group, IGF-1 group, IGF-1＋NG-nitro-L-arginine methyl ester (L-NAME) group and L-NAME group. Cells were cultured with EGM2 for 2 to 3 weeks, and the proliferation and adhesion function of EPC were determined in each group. Results The more severe the degree of carotid stenosis, the lower the number of EPC colony forming (P＜0.05), the lower the serum IGF-1 concentration, and the proliferation and adhesion ability of EPC decreased with the increase of the degree of stenosis. Function experiments showed that EPC function in IGF-1 group was significantly higher than that in untreated group (P＜0.01), IGF-1＋L-NAME group had no obvious difference, and EPC function in L-NAME group was lower than that in untreated group. The endothelial nitric oxide synthase (eNOS) in IGF-1 group was significantly higher than that in untreated group, there was no significant difference in IGF-1＋L-NAME group, and eNOS in L-NAME group was lower than that in untreated group. Conclusion EPC may have a protective effect on carotid stenosis, and IGF-1 may enhance the function of EPC by affecting the synthesis of eNOS.

Abstract:Aim To investigate the dynamic changes of circulating endothelial progenitor cells(EPC) counts after percutaneous coronary intervention(PCI) in patients with chronic stable angina pectoris and related factors of CD34⁺/KDR⁺ maximum motivation. Methods 93 patients were divided into PCI group (n=72) and control group (n=21).Blood samples were collected by femoral artery sheath or median cubital vein. EPC counts were measured following CAG(baseline) and 1 h, 3 h, 5 h, 7 h, 24 h after PCI or CAG by flow cytometry. Results Population means of different type EPC counts has significantly statistic difference at different time points and EPC counts between PCI group and control group(P＜0.05). In PCI group, CD34⁺/KDR⁺ at 24 h, CD133-/CD34⁺/KDR⁺ at 3 h, 5 h, 24 h, CD133⁺/CD34⁺/KDR⁺ at 5 h, 7 h, CD133⁺/KDR⁺ at 3 h, 5 h, CD133⁺/CD34⁺ at 24 h has significantly statisitc difference compared with baseline(P＜0.05). However, there has no significantly statisitc difference in the counts of each type of EPC at different time points compared with baseline in the control group(P＞0.05). The maximum motivation of CD34⁺/KDR⁺ has negative relationship with basal C-reactive protein, and has positive correlations with body mass index (BMI), angiotensin-converting enzyme inhibitor (ACEI) or angiotensin Ⅱ receptor antagonists (ARB) drug treatment and the quantitative parameters of endothelial injury. Conclusion PCI can initiate time-dependment mobilization of EPC and promote motivation, migration and recruitment of CD34⁺/KDR⁺ which can accelerate endothelial damage reparation and reduce complication of patients with chronic stable angina pectoris after PCI to improve prognosis.

Abstract:Aim To investigate the relationship between coronary artery lesion and carotid atherosclerosis (CAS), cerebral infarction in patients with coronary heart disease. Methods 319 patients with coronary heart disease diagnosed by coronary angiography were selected. The patients with coronary heart disease were divided into four groups according to the degree of coronary artery lesion. The differences of CAS grade score, Crouse plaque score, plaque number, and cerebral infarction incidence were compared in each group. In addition, 319 cases of coronary heart disease were divided into two groups:cerebral infarction group and non cerebral infarction group, according to whether there was cerebral infarction or no. The differences of carotid plaque character, CAS grade score, Crouse plaque score, plaque number were compared between two groups. Results The CAS grade score, Crouse plaque score, plaque number in 3 branchs lesion group and left main coronary lesion group were significantly higher than those in 1 branch lesion group and 2 branchs lesion group (P＜0.05). The incidence of cerebral infarction was 27.53% in 3 branchs lesion group, and the incidence rate was 38.27% in left main coronary lesion group. Cerebral infarction case was not found in 1 branch lesion group and 2 branchs lesion group. The incidence of unstable plaque in the cerebral infarction group was significantly higher than that in the non cerebral infarction group (90.00% vs 46.02%, χ²＝6.2949, P＜0.05). Conclusions In patient with coronary heart disease, the more serious the coronary artery lesion, the more severe the CAS, the higher the incidence of cerebral infarction. Carotid unstable plaque is more likely to induce cerebral infarction.

Abstract:Aim To analyze the changes of the parameters of central aortic pressure and arterial stiffness in hypertensive patients with different stages of menopause; To investigate the protective effect of estrogen on cardiovascular system in female. Methods 118 patients with hypertension were selected, and 51 cases were female and 67 cases were male. According to menopausal years, female patients were divided into short-term menopause group (menopause time was less than 5 years) and long-term menopause group (menopause time was more than 5 years). Male patients whose age were consistent with the above two female groups, were as short-term control group and long-term control group. Peripheral arterial systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP) were detected.Central systolic blood pressure (cSBP), central diastolic blood pressure (cDBP), central pulse pressure (cPP), augmentation pressure (AP), central aortic pressure augmentation index (AIx), augmentation index adjusting for a heart rate of 75 beats/min (AIx75HR) and carotid-femoral pulse wave velocity (cfPWV) were measured. Results (1)SBP, DBP, cSBP, cDBP and cfPWV in short-term menopause group were lower than those in short-term control group, AP, cPP, AIx and AIx75HR in short-term menopause group were higher than those in short-term control group, and the differences of SBP, DBP, cDBP, AIx75HR between the two groups were statistically significant (P＜0.05). (2)SBP, PP, heart rate, cSBP, cPP, AP, AIx, AIx75HR and cfPWV in long-term menopause group were larger than those in long-term control group, and the differences of SBP, PP, cSBP, cPP, AP, AIx75HR between the two groups were statistically significant (P＜0.05). (3)The levels of estradiol and progesterone in short-term menopause group were higher than those in long-term menopause group, and the difference of estradiol level between the two groups was statistically significant (P＜0.05). Conclusions Estrogen level in hypertensive female with short-term menopause can maintain the protection of cardiovascular system. Estrogen has a protective effect on not only peripheral blood pressure but also central aortic pressure, but its protective effect is not obvious on arterial stiffness.

Abstract:Aim To investigate the protective effect of olmesartan on vascular endothelial function in patients with hypertension complicated with coronary heart disease and diabetes mellitus, by observing the change of vascular endothelial function before and after treatment with olmesartan. Methods 160 cases of hypertensive patients were collected, and according to whether complicated with coronary heart disease and diabetes mellitus, the patients were divided into 3 groups:pure hypertension group (H group, n＝40), hypertension complicated with coronary heart disease group (HC group, n＝62) and hypertension complicated with coronary heart disease and diabetes mellitus group (HCD group, n＝58). And then each group was divided into 2 subgroups:olmesartan intervention subgroup (A subgroup) and and non olmesartan intervention subgroup (B subgroup). Baseline data and general examination indicators of each group were counted. Enzyme-linked immunosorbent assay was used to detect the concentration of serum nitric oxide (NO) and endothelin-1 (ET-1). The number of peripheral blood endothelial progenitor cell (EPC) was detected by flow cytometry.Above indicators were reexamined after intervention with olmesartan for 3 months. Results (1)Vascular endothelial relaxing and contracting factors:Before treatment, compared with H group, NO concentration was significantly lower, while ET-1 concentration was significantly increased in HC group and HCD group, and the change of HCD group was more obvious (P＜0.05). After treatment, compared with before treatment, NO concentration was significantly increased, while ET-1 concentration was decreased in HC-A subgroup and HCD-A subgroup (P＜0.05). (2) EPC number of peripheral blood:Before treatment, compared with H group, the EPC number of peripheral blood was significantly decreased in HC group and HCD group, and the decrease of HCD group was more obvious (P＜0.05). After treatment, compared with before treatment, the number of EPC was significantly increased in HC-A subgroup and HCD-A subgroup (P＜0.05). Conclusions Hypertensive patients complicated with coronary heart disease and diabetes mellitus will increase the damage of vascular endothelium. Olmesartan can inhibit the imbalance of vascular endothelial relaxing and contracting factors, increase the EPC number of peripheral blood, and it has protective effect to vascular endothelium.

Abstract:Aim To assess the prevalence of metabolic syndrome and correlative risk factors among the middle-aged and elderly populations in Chengyu area. Methods In 2013, a total of 7807 middle-aged and elder adults aged 40-79 years were enrolled from Chengyu area using a stratified cluster sampling method, to check height, weight, blood pressure, blood fat and oral glucose tolerance test (OGTT), etc. Data were collected through questionnaire and the diagnostic criteria for using the Chinese Medical Association standard complications. Results The prevalence of metabolic syndrome was 13.8%. Male and female prevalence was 13.3% and 14.1%, the prevalence of the sexes had no statistical difference. The urban and rural prevalence was 14.6% and 10.6%, the urban prevalence rate was higher than the rural. There was an increasing prevalence with the increase of age, but it fell slightly above 70-years-old. Age, abdominal obesity, lack of physical exercise were major related factors of metabolic syndrome among middle-aged and elderly male in Chengyu area; Age, family history of hypertension, abdominal obesity were related factors of metabolic syndrome among middle-aged and elderly female. Conclusion There was a high prevalence of metabolic syndrome among the middle-aged and elder adults in Chengyu area. It was important to control reasonable waist circumference for metabolic syndrome prevention and intervention of the crowd and prevent the occurrence and development of cardiovascular disease.

Abstract:Sustained hyperglycemia is the basic feature of insulin resistance and type 2 diabetes. Disorders of glucose homeostasis lead to metabolic dysfunction, thus provoking diabetes and diabetic complications. Sirtuin 1 (Sirt1), a mammalian NAD-dependent protein deacetylase, plays a critical role in energy metabolism and insulin resistance. Recent studies suggest that activation of Sirt1 deacetylates various proteins such as PGC-1α, NF-κB, Foxo1 and Akt, which in turn protects pancreatic β cell functions, improves insulin sensitivity, attenuates inflammation and subsequently maintains glucose homeostasis. This review summarizes recent advances in the role of Sirt1 in regulating glucose homeostasis.

Abstract:Atherosclerosis (As) is a chronic disease involving several kinds of cells and induced by a variety of factors. The proliferation and migration of vascular smooth muscle cell (VSMC) have an important influence on the occurrence and development of As, including the promotion of the plaque formation and the instability of the plaque. Conversion of VSMC from contractile phenotype to synthetic phenotype is the basis of VSMC proliferation and migration. The maintanance of VSMC contractile phenotype is helpful to inhibit its abnormal proliferation and the plaque formation. Myocardin, as the key transcription factors of VSMC contraction marker genes, binds to serum response factor to facilitate expression of VSMC contraction marker genes. Many kinds of functional factors such as estrogen receptor α, histone modification, DNA methylation and microRNA, can be combined with myocardin, regulating vascular function and inhibiting the phenotype switch of VSMC; various channels, such as transforming growth factor-β1 and platelet derived growth factor-BB signaling pathway, can increase expression of myocardin to inhibit the proliferation and migration of VSMC. So myocardin plays an important role in the development of As. Regulating myocardin to affect the phenotype switch of VSMC may become a new therapeutic strategy for As and other cardiovascular diseases in the future.

Abstract:A large number of clinical epidemiological studies have shown that high density lipoprotein (HDL) level is inversely associated with cardiovascular disease risk factors. Apolipoprotein AⅠ (ApoAⅠ) is the main functional protein in HDL, and the content of HDL is about 70%. Oligo-lipid ApoAⅠ is the main recipient of ATP-binding cassette transporters (ABCA1) mediated cholesterol efflux from macrophages. It can mediate cholesterol efflux free from macrophage, then start reverse cholesterol transport (RCT) process, and remove excess cholesterol in extrahepatic tissue. A large number of animal experiments have also confirmed that the lack of HDL ApoAⅠcan also lead to the increase of atherosclerosis, and overexpression of human ApoAⅠgene can significantly inhibit the generation of early atherosclerosis in mice. The mechanisms of ApoAⅠ gene expression and the related factors of inducing and inhibiting ApoA Ⅰexpression will be reviewed in this article.

Abstract:Arteriosclerosis obliterans (ASO) has become a serious threat to people's physical and mental health of primary peripheral vascular disease, and early diagnosis and treatment is urgent and necessary. In recent years, as the research on the non-protein mechanism of post-transcriptional mechanism become clear, part of the research focused on exploring the relationship between microRNA and ASO. Therefore, this paper based on the regulation of microRNA in atherosclerosis model, animal model and patients with vascular smooth muscle cells proliferation, migration, differentiation, phenotypic transformation, apoptosis, senescence, inflammation and oxidative stress related to learning and research. From the aspects of gene regulation, microRNA research could better explain the occurrence and development of hardening of the ASO, but because of the many factors, such as complicated regulatory mechanism and the lack of the pharmacokinetics and pharmacodynamics research data, many target genes and so on, its clinical application is still restricted. In the future, the microRNA healing potion applied to the treatment of vascular diseases, especially in lower limb arteriosclerosis occlusion disorder will reduce the damage effectively.