Abstract:Recent studies have shown that angiotensin-converting enzyme-2 (ACE2) plays an important role in the pathogenesis of atherosclerosis, aneurysm, coronary heart disease, diabetic cardiomyopathy and adriamycin cardiomyopathy. There is increasing support for the belief that ACE2 has a significant role in inhibiting vascular and myocardial remodeling, which is of great significance in the prevention and treatment of cardiovascular diseases.

Abstract:Aim To observe the effect of angiotensin(1-7) (Ang(1-7)) on myocardial apoptosis, and investigate the underlying mechanism. Methods H9c2 cells were treated by isoproterenol (ISO) for 12 h to eastablish a model of apoptosis. Co-treatment of Ang(1-7) or PI3K inhibitor (LY294002) with ISO or ISO and Ang(1-7) for 12 h was performed to observe the influence on ISO-induced myocardial apoptosis. The cell growth state was observed under white light. MTS was used to detect the relative cellular activity. The apoptotic rate was tested by TUNEL under fluorescence microscope. The mitochondrial transmembrane potential was detected by fluorescence probe JC-1. The protein expression of cleaved Caspase-3, p-Akt and Akt were tested by Western blot. Results ISO inhibited the relative activity of H9c2 cells. Ang(1-7) reversed the ISO-induced cellular activity reduction of H9c2 cells concentration-dependently. Compared with control group, apoptosis rate and the protein expression of cleaved Caspase-3 increased significantly in ISO group, and the mitochondrial transmembrane potential and the protein expression of p-Akt decreased notably. Ang (1-7) could inhibit the increasing of apoptosic rate and the protein expression of cleaved Caspase-3, promote mitochondrial transmembrane potential and the protein expression of p-Akt in ISO-indcued H9c2 cell. The protective effect of Ang(1-7) on ISO-induced apoptosis was markedly reduced by pretreatment with LY294002, evidenced by increasing in apoptosic rate and the protein expression of cleaved Caspase-3, decreasing in the protein expression of p-Akt. Conclusion ISO induces apoptosis by decreasing mitochondrial transmembrane potential. Ang(1-7) could reverse this effect. Ang(1-7) protecting H9c2 cells from ISO-induced apoptosis may relate to PI3K/Akt signal pathway.

Abstract:Aim To observe the effect of Huayu Qutan recipe on regulating the expression of HIF-1α/VEGF/VEGFR-2 pathway on the aortic lipid plaque in As rabbits and to explore the mechanism of the Huayu Qutan recipe on the atherosclerotic plaque. Methods Sixty New Zealand rabbits were randomly divided into the control group (n=15) and the experimental group (n=45). Rabbits in the experimental group were prepared as atherosclerotic rabbit model by immune-induced endothelial injury and by feeding with high-fat diet. The control group was given normal feed. After 8 weeks, the rabbits in the experimental group were randomly divided into the model group, the Huayu Qutan recipe group and the Simvastatin group. Each group was given the corresponding drug intervention; the control group and the model group were given the same volume of saline, one time a day for 4 weeks before taking materials. The levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDLC) and high-density lipoprotein cholesterol (HDLC) in serum were detected by the automatic biochemical analyzer. HE staining and the oil red O staining were used to observe the pathological changes of the aorta in rabbits. The thickness of the intima and tunica media was measured in aortic wall. Immunohistochemical method was adopted to determine CD31 mean optical density value. The contents of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor(VEGF) in serum were detected by ELISA. Western blot was used to detect the expression of HIF-1α, VEGF and VEGFR-2 in the aorta. Results Compared with the control group, the levels of TG, TC and LDLC in the model group were significantly increased (P<0.01) and HDLC levels were significantly decreased (P<0.01). Compared with the model group, the levels of TG, TC and LDLC in the Huayu Qutan recipe group and the Simvastatin group were significantly decreased (P<0.05 or P<0.01), and HDLC content was significantly increased (P<0.05 or P<0.01). Compared with the control group, the thickness of intima and tunica media were significantly increased in the model group (P<0.01) . Compared with the model group, the thickness of intima and tunica media were significantly decreased in the Huayu Qutan recipe group and the Simvastatin group (P<0.01). Compared with the control group, the CD31 mean optical density value were significantly increased in the model group (P<0.01). Compared with the model group, the CD31 mean optical density value were significantly decreased in the Huayu Qutan recipe group and the Simvastatin group (P<0.01). Pathological staining showed the aortic intimal hyperplasia, a large number of foam cells and lipid deposition in the model group. After the treatment of the Huayu Qutan recipe and the simvastatin, they were significantly improved. Compared with the control group, the contents of HIF-1α and VEGF were significantly increased in the model group (P<0.01). Compared with the model group, the levels of HIF-1α and VEGF were significantly decreased in the Huayu Qutan recipe group and the Simvastatin group (P<0.05 or P<0.01). The expressions of HIF-1α, VEGF and VEGFR-2 in the aorta of the model group were significantly higher than those in the normal group (P<0.01). After treated by the Huatan Qutan recipe and the Simvastatin, the expression of HIF-1α, VEGF and VEGFR-2 in the two groups were significantly lower than those in model group (P<0.01). Conclusion The Huayu Qutan recipe stabilizes the As lipid plaque and the mechanism may be related to the regulation of HIF-1α / VEGF / VEGFR-2 pathway to inhibit angiogenesis.

Abstract:Aim To investigate the effect of cladribine (2-CdA) on the viability, migration, cell cycle and secretion activity of human umbilical vein endothelial cells, and to evaluate the influence of 2-CdA on cardiovascular system in clinical application. Methods The effect of different concentrations of 2-CdA on the growth of endothelial cells was detected by CCK-8. The cell migration ability was detected by scratch test. The cell cycle was analyzed by flow cytometry. The cell apoptosis was detected by acridine orange and ethidium bromide. The content of nitric oxide (NO) was determined by Gries method. ELISA method was used to detect vascular endothelial growth factor (VEGF) level. Results In the concentration range of 0.4 to 40 mol/L, 2-CdA had an obvious inhibitory effect on endothelial cells, and IC50 was 4.126 mol/L. With the increase of drug concentration and the prolongation of action time, the inhibitory effect of 2-CdA increased. High concentration of 2-CdA for a long time could induce endothelial cell apoptosis. After 5 μmol/L 2-CdA acted on endothelial cells, the migration ability of cells was inhibited, and the cell cycle was significantly blocked in S phase. The staining results of acridine orange and ethidium bromide showed that high concentration of 2-CdA could induce apoptosis of endothelial cells. After the action of 5 μmol/L 2-CdA on endothelial cells, NO and VEGF contents were reduced. Conclusion 2-CdA has the toxic effect of endothelial cells, resulting in cell cycle arrest and cell apoptosis.

Abstract:Aim To investigate the protection effect of microRNA-22 on cardiac function and ventricular remodeling after myocardial infarction. Methods The study constructed mouse myocardial infarction model and transfected adenovirus containing microRNA-22 into peri-infarct area. It assessed cardiac function four weeks after myocardial infarction by using echocardiography. Mouse exercise ability was assessed by swimming. HE and Masson staining was applied to assess microstructure and fibrosis of myocardium. Results Over-expressing of microRNA-22 improved mouse left ventricular ejection fraction (LVEF) percentage (49.38%±2.51% vs 42.29%±2.74%, P<0.05) and fractional shortening (FS) percentage (24.24±0.64% vs 22.59%±0.73%, P<0.05) compared with adeno-null group. Mouse in adeno-microRNA-22 group showed longer swimming time and better exercise ability (8.13±1.01 min vs 7.02±1.32 min, P<0.05).HE and Masson staining also showed better cardiac microstructure and less fibrosis. Adeno-microRNA-22 group showed elevated microRNA-22 expression (6.66±2.01 vs 1.22±0.07, P<0.05) and down-regulated PTEN protein expression (0.63±0.19 vs 2.23±0.44, P<0.05). Conclusion Over-expression of microRNA-22 protected mouse cardiac function and reduced ventricular remodeling after myocardial infarction.

Abstract:Aim To synthetize a nuclear magnetic resonance imaging (MRI) nano contrast agent targeted to atherosclerosis (As) lesions, and to provide experimental evidence for the development of a new MRI diagnostic technique for As. Methods The self developed aptamer PM1, which was targeted to the foam cells, was coupled to iron oxide (Fe₃O₄) nanoparticles, and the target MRI contrast agent was prepared, named MRI-As. The As animal model of apolipoprotein E gene knockout (ApoE－/－) was established by feeding with high-fat diet. The As lesion of aorta was identified by Sudan red Ⅳ staining. Effect of MRI-As contrast agent on MRI imaging of plaque in As mice was detected by MRI imager. Results MRI imaging of the ApoE－/－ mice animal model showed that the aortic wall was rough. As lesions showed high signal intensity, which was well contrasted with the surrounding tissues. The central signal was higher, more uniform and the edge was clearer. After injection of MRI-As contrast agent, the signal intensity of As lesion area showed a downward trend, and the vascular wall was not smooth and showed the defect of multiple spot signal. After injection of MRI-As contrast agent in control group, the signal intensity of vascular wall did not change significantly. ConclusionsMRI-As contrast agent can play an active targeting to As lesions. Using the negative contrast effect of Fe₃O₄ nanoparticles on As lesions, MRI-As contrast agent significantly enhances the resolution of the MRI image of As lesion, and it has the potential of new, fast, efficient, non-invasive, non radiative contrast agent for As MRI image.

Abstract:Aim To explore the effects and mechanisms of transplantation of macrophages transfected with heme oxygenase-1 (HO-1) gene by adenovirus vectors on inflammation, oxidative stress in acute myocardial infarction (AMI) area. Methods Rat alveolar macrophages were cultured in vitro and divided into three groups and treated differently:control group, the cells were not transfected with adenovirus; Ad-Mφ group, the cells were transfected with blank adenovirus vector; Ad-HO-1-Mφ group, the cells were transfected with adenovirus carrying the HO-1 gene. The proliferative activity of macrophages and the expression of HO-1 protein as well as the inflammatory cytokines such as tumor necrosis factor (TNF-α), interleukelin-6 (IL-6), IL-10 in the supernatant were detected. In addition, The AMI model in rats were established by ligating coronary artery and randomly divided into three groups:the simple AMI group, the Ad-Mφ transplantation group and the Ad-HO-1-Mφ transplantation group. PBS, PBS containing 2×10⁵ Ad-Mφ and PBS containing 2×10⁵ Ad-HO-1-Mφ were injected into the myocardial infarction area of rats in each group respectively. 5 days later, the expression of HO-1 protein and the inflammatory cytokines such as IL-12, TNF-α, IL-10, monocyte chemotactic protein 1 (MCP-1) as well as the total antioxidant capacity (T-AOC) and malondialdehyde (MDA) content in infarcted myocardium were detected. Results Adenovirus transfection itself did not affect macrophage proliferation activity, but could transfer HO-1 gene into macrophage and obtain high expression. Ad-HO-1-Mφ could significantly reduce the expression of pro-inflammatory cytokine TNF-α, IL-6 and increase the expression of anti-inflammatory factor IL-10 (P<0.05). Compared with the simple AMI group and the Ad-Mφ transplantation group, the infarcted area of Ad-HO-1-Mφ transplantation group showed much more expression of HO-1 protein and IL-10 and less expression of TNF-α, IL-12, MCP-1 while T-AOC increased and MDA content decreased significantly (P<0.05 respectively). Conclusion Ad-HO-1-Mφ could overexpress HO-1 protein and polarize into M2 phenotype which has powerful anti-inflammatory properties. After being transplanted into myocardial infarcted area, the Ad-HO-1-Mφ could still overexpress HO-1 protein and significantly reduce the inflammation and oxidative stress levels in myocardial infracted area.

Abstract:Aim To investigate the effect of Ligustrazine injection on myocardial injury markers and cardiac function in rats with acute myocardial infarction. Methods 36 male SD rats were selected as experimental animal and randomly divided into control group, model group and intervention group, 12 animals in each group. Model group and intervention group were used to establish acute myocardial infarction (AMI) model, and intervention group was treated with ligustrazine injection. At 1 week and 3 weeks after intervention, the cardiac color doppler echocardiography was performed to measure the cardiac function, and serum was collected for the determination of myocardial injury markers and oxidative stress indexes. Results 10 rats were survived in each group. At 1 week and 3 weeks after intervention, left ventricular end-diastolic diameter (LVEDd) and left ventricular end-systolic dimension (LVESd) in model group were significantly higher than those in control group, and left ventricular ejection fraction (LVEF) in model group was significantly lower than that in control group (P＜0.05); LVEDd and LVESd in intervention group were significantly lower than those in model group, and LVEF was significantly higher in intervention group than that in model group (P＜0.05). At 1 week after intervention, serum creatine kinase isoenzyme MB (CK-MB), cardiac troponin I (cTnI) and cardiac troponin T (cTnT) contents in model group were significantly higher than those in control group (P＜0.05); Serum CK-MB, cTnI, cTnT contents in intervention group were significantly lower than those in model group (P＜0.05). At 3 weeks after intervention, serum cTnI and cTnT contents in model group were significantly higher than those in control group (P＜0.05); Serum cTnI and cTnT contents in intervention group were significantly lower than those in model group (P＜0.05). At 1 week and 3 weeks after intervention, serum malondialdehyde (MDA) contents in model group was significantly higher than that in control group, and serum superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) contents were significantly lower than those in control group (P＜0.05); Serum MDA contents in intervention group was significantly lower than that in model group, and serum SOD and GSH-Px contents were significantly higher than those in model group (P＜0.05). Conclusion Ligustrazine injection can reduce myocardial cells injury and oxidative stress reaction and improve cardiac function in AMI rats.

Abstract:Aim To investigate the expression of swiprosin-1 in atherosclerotic tissue and its influence on apoptosis and inflammatory factors expression in macrophages. Methods Establishment of atherosclerosis mouse model, RT-PCR and Western blot were used to detect the expression of swiprosin-1 in atherosclerotic tissues. Treatment of macrophage THP-1, smooth muscle cell VSMC, endothelial cell EC-304 with ox-LDL, the expression levels of swiprosin-1 were detected by RT-PCR and Western blot. Macrophage THP-1 was transfected with swiprosin-1 siRNA, and siRNA control, after ox-LDL treatment, apoptosis was detected by flow cytometry, the expression of cleaved Caspase-3 and cleaved Caspase-9 were detected by Western blot, TNF-α and IL-6 in the supernatant of culture medium were detected by ELISA.Results The expression level of swiprosin-1 in atherosclerotic tissue was higher than that in normal tissue. The expression level of swiprosin-1 in macrophage THP-1 after ox-LDL treatment was the highest, in smooth muscle cell VSMC and endothelial cell EC-304 were very low. The apoptotic rate of macrophage THP-1 treated with ox-LDL was as high as 21.64%±1.88%, the expression levels of cleaved Caspase-3 and cleaved Caspase-9 in cells were increased, the levels of TNF-α and IL-6 in the supernatant of culture medium were also significantly increased. The apoptotic rate of macrophage THP-1 treated by ox-LDL after swiprosin-1 interference decreased to 15.25%±1.10%, the expression levels of cleaved Caspase-3 and cleaved Caspase-9 in cells were decreased, the contents of TNF-α and IL-6 in the supernatant of culture medium also decreased obviously. Conclusion Elevated expression of swiprosin-1 in atherosclerotic tissue, reducing swiprosin-1 expression could inhibit apoptosis and inflammatory cytokine secretion in macrophages induced by ox-LDL.

Abstract:Aim To study the protective effect of curcumin on vascular calcification in rat model. Methods30 male SD rats were randomly divided into 3 groups, 10 in each group, namely the control group, the calcification group and the intervention group. Vitamin D3 and nicotine were used to establish vascular calcification model. Vascular calcification was detected by von Kossa staining, calcium content and the activity of alkaline phosphatase (ALP) were detected by kit, Western blot was used to detect the protein expression of bone morphogenetic protein-2 (BMP-2), Runx2 and cathepsin D (CTSD), immunohistochemical staining was used to observe the expression and distribution of CTSD in blood vessels. Results Vitamin D3 and nicotine could induce vascular calcification, increase calcium content and the activity of ALP, and upregulate the expression of BMP-2 and Runx2. Meanwhile, curcumin could play a protective effect against the vascular calcification, decrease calcium content and the activity of ALP, and downregulate the expression of BMP-2 and Runx2 induced by Vitamin D3 and nicotine. Furthermore, CTSD was upregulated and distributed in extracellular matrix after treated with Vitamin D3 and nicotine. Curcumin could downregulate the expression of CTSD and reduce its distribution in extracellular matrix. Conclusion Curcumin could inhibit vascular calcification in rat model induced by vitamin D3 and nicotine and it may play protective role via regulating the expression of CTSD.

Abstract:Aim To investigate the changes of serum miR-24 and its target gene YKL-40 in diabetes mellitus (DM) with coronary heart disease (CHD) and explore its clinical significance as a predictive potential biomarker. Methods According to the coronary arteries angiography and diabetes diagnostic criteria, the study included 61 subjects with CHD subjects (n=34), DM+CHD subjects (n=27), and 32 negative predictive value of coronary angiography (control) in our affiliated hospital from October 2013 to June 2016. Gensini score was used to evaluate the severity of coronary artery lesions. Bioinformatic analysis and identification of serum miR-24 and its target YKL-40 were assessed using quantitative real-time PCR, ELISA after a bicinchoninic acid (BCA) assay, and receiver-operating characteristic (ROC) assays. Results miR-24 was especially gradually decreased in serum of CHD and DM+CHD patients compared with controls and reached to minimum in DM+CHD groups, and conversely, its target YKL-40 mRNA and protein levels were significantly increased in serum of CHD and DM+CHD patients and reached to maximum in DM+CHD groups. Furthermore, the area under the curve (AUC) and 95% confidence interval (CI) for the receiver-operating characteristic (ROC) analysis was 0.919 (95% CI:0.856～0.983) and 0.901 (95%CI:0.814～0.988), suggesting that the levels of miR-24 have high diagnostic values in distinguishing between DM+CHD and non-DM+CHD, or DM+CHD and CHD. Conclusions Serum circulating miR-24 was significantly decreased in patients with DM+CHD that had high clinical diagnostic value, indicating that miR-24 could be a potential biomarker for predicting diabetes mellitus with coronary heart disease.

Abstract:Aim To investigate the relationship between serum uric acid on admission and incidence of contrast-induced nephropathy (CIN) in patients with coronary heart disease complicated with diabetes mellitus. Methods A total of 150 patients with coronary heart disease complicated with diabetes mellitus were divided into two groups:control group (n=95) and increased serum uric acid group (n=55). The incidence of CIN was compared between the two groups and the risk factors of CIN were analyzed by Logistic regression. Results The incidence of CIN in 55 patients with increased serum uric acid was 27.27% (15/55),and it was significantly higher than that in patients with normal serum uric acid [10.53%(10/95), P=0.008]. Multivariate Logistic regression analysis revealed that the independent risk factors of CIN were serum uric acid (OR 1.7,5% confidence interval:1.001～1.013, P=0.014) and contrast dosage (OR 1.5,5% confidence interval:1.017～1.054, P=0.000). Conclusion Increased serum uric acid on admission is independently associated with higher risk of CIN among patients with coronary heart disease complicated with diabetes mellitus.

Abstract:Aim To study the efficacy and safety of ibutilide for immediate cardioversion of recent-onset persistent atrial fibrillation (PAF) in elderly patients (＞65 years) with left ventricular dysfunction (LVD). Methods 100 elderly patients of recent-onset PAF with LVD were hospitalized in our department of Cardiology from January 2014 to August 2017, and divided into two groups by random number table method:ibutilide group (50 cases) were treated with ibutilide intravenous injection on conversion, initial dose was 1 mg, slow injection after dilution； amiodarone group (50 cases) were treated with amiodarone intravenous injection on conversion, initial dose was 150 mg, slow injection after dilution. The cardioversion rates were compared between the two groups within 30 min, 60 min, 4 hours and 24 hours, the left ventricular function indexes (LVEDD, LVESD, LVEF and NT-proBNP) were measured before treatment and 48 hours after treatment, and adverse events were recorded in the two groups during the conversion (within 24 hours). Results The cardioversion rates of PAF in the ibutilide group were higher than those in the amiodarone group within 30 min, 60 min, 4 hours and 24 hours (P＜0.01 or P＜0.05), the average cardioversion time of PAF in the ibutilide group were shorter than that in the amiodarone group (t＝－3.232, P＝0.002). QTc average recovery time in the ibutilide group were shorter than that in the amiodarone group (t＝－17.743, P＝0.000). LVEDD, LVESD, LVEF and NT-proBNP were significantly improved in the two groups compared with before treatment and 48 hours after treatment (P＜0.01 or P＜0.05), the ibutilide group improved more significantly (P＜0.01 or P＜0.05). The incidence of short-term adverse reactions in the ibutilide group was lower than that in the amiodarone group (χ²＝4.762, P＝0.029), the duration of adverse events in the ibutilide group were shorter than that in the amiodarone group (P＝－11.622, P＝0.000). Conclusion Compared with amiodarone, ibutilide was used in the treatment of recent-onset PAF in elderly patients with LVD, with rapid onset, high conversion rate, significant improvement in LVD and good safety.

Abstract:Aim To observe the level of apolipoprotein CⅢ(ApoCⅢ) in the serum between the patients with acute myocardial infarction and non-coronary heart disease whether they were significantly different, and to explore its clinical significance. Methods A total of 110 patients were enrolled. They were divided into acute myocardial infarction group and non-coronary heart disease group, including 84 people in acute myocardial infarction group, and 26 people in non-coronary heart disease group. The clinical data of patients during hospitalization were collected, including general information such as age, sex, hypertension, diabetes mellitus, dyslipidemia, smoking history, and blood biochemical index data, including serum troponin I(cTnI), triglyceride(TG), total cholesterol(TC), low density lipoprotein cholesterol (LDLC), high density lipoprotein cholesterol (HDLC), uric acid(UA), homocysteine, serum brain natriuretic peptide (BNP), ejection fraction (EF), and serum inflammation index data, including serum cystatin C (CysC) and high-sensitivity C-reactive protein (hs-CRP). The levels of serum apolipoprotein CⅢ in each patient were measured. Results Compared with non-coronary heart disease group (P<0.05), there were more males in the myocardial infarction group, and smoking rate was higher than that of non-coronary heart disease group (P<0.05). Serum cTnI and serum BNP in patients with myocardial infarction were higher than those in non-coronary heart disease group (P<0.05), while HDLC and EF were lower than those of non-coronary heart disease group (P<0.05). The levels of serum CysC, hs-CRP and apolipoprotein CⅢ in the myocardial infarction group were significantly higher than those in the non-coronary heart disease group (P<0.01). Multivariate linear regression analysis showed that there was no significant correlation between apolipoprotein CIII and sex, smoking history, HDLC, cTnI, BNP, EF, CysC, hs-CRP which were significantly different between the two groups. Conclusion The levels of serum apolipoprotein CⅢ in patients with acute myocardial infarction were significantly higher than those in patients without coronary heart disease. Considering that apolipoprotein CⅢ promotes the formation of atherosclerosis by affecting blood lipid metabolism and the process involves a variety of inflammatory mediators, apolipoprotein CⅢ may be a predictor of inflammatory response to acute myocardial infarction.

Abstract:Urotensin Ⅱ is a kind of potent cyclic neuropeptide and has a series of biomedical functions. Recent studies have identified that the upregulation of urotensin Ⅱ and UT are involved in the process of organ fibrosis. The mechanisms of UⅡ effects are complicated and a number of signaling pathways activated by urotensin Ⅱ are related to myocardial fibrosis. This study reviewed the physiological and pathophysiological effects of urotensin Ⅱ involved in organ fibrosis, focusing on the correlation between urotensin Ⅱ and the concerned signaling pathways on myocardial fibrosis.

Abstract:Arteriosclerosis obliterans of lower extremity (ASO) is caused by atherosclerosis and characterized by arterial stenosis and occlusion. Endovascular stenting as a minimally invasive, safe and effective method, has been widely used in the femoral artery and popliteal artery ASO treatment. However, the incidence of restenosis (ISR) in the stent is high, which seriously affects the clinical prognosis of the patients. Stent restenosis remains a major problem in stent use. In this paper, the mechanism, risk factors and the latest treatment progress of restenosis after stent implantation are reviewed, which is of significance to the prevention and treatment of ISR.

Abstract:Atherosclerosis (As) is closely related to lipid metabolism disorder and inflammation. The current study shows that intestinal microbial flora is also involved in the As process and is one of the independent risk factors of As.The human gut is the largest digestive organ and “the largest immune organ” of the body. Normal intestinal flora participates in bile acid metabolism, and the short-chain fatty acids produced by bacterial metabolism inhibit inflammation, thus suppressing As. Unbalanced intestinal flora affects trimethylamine metabolic pathway of the host, disturbs the metabolism of cholesterol in the body, triggers the innate and adaptive immune responses, and attenuates the protective effect of anti-inflammatory, thus promoting As. Therefore, the regulation of unbalanced intestinal flora becomes a new target for the treatment of As. This article will review the immune mechanism of intestinal flora affecting As.

Abstract:Atherosclerosis (As) is a kind of chronic inflammatory disease, which characterized by the deposition of lipid in vessel wall. Chronic inflammation of vascular wall induced by As factors plays an important role in the pathophysiological process of the disease. The reprogramming of energy metabolism of monocytes/macrophages is closely related to the occurrence and development of As. Warburg effect is an important way of cell energy metabolism. This effect may be involved in some pathological processes of As, such as vascular smooth muscle proliferation, endothelial cell dysfunction, and inflammation. This article reviews the Warburg effect of the vascular wall in As.